bluuebunny/crossref_metadata_2025 huggingface dataset:
IgE production in rat fascioliasis
Authors: PFISTER K. , TURNER K. , CURRIE A. , HALL E. , JARRETT E.E.E.
Published: October 2007

Summary F. hepatica infection of rats caused a prolonged elevation of serum total IgE reflecting the continued presence of live worms in the host. Infection with 40 metacercariae stimulated higher total IgE levels than infection with 20 metacer‐cariae. The parasite specific IgE response was biphasic, the first peak coinciding with the migratory phase in the liver parenchyma and the second with the establishment of flukes in the bile ducts.
Immunological detection of Plasmodium knowlesi antigens after electrophoretic transfer from SDS‐polyacrylamide gels to diazophenylthioether paper
Authors: JOHNSON DIANA M. A. , COHEN S.
Published: October 2007

Summary Freeze‐thawed extracts of mature schizonts of Plasmodium knowlesi (strain Wl) were electrophoresed in sodium dodecylsulphate (SDS) polyacryl‐amide gels, then transferred electrophoretically to diazophenylthioether paper. The transferred antigen was probed using a purified polyvalent, polyclonal immune serum pool isolated from rhesus monkeys (Macaca mulatto). This method for identifying parasite antigens was compared with immunoabsorption, using parasites which had been metabolically labelled in vitro with 35S‐methionine. The methods showed general correspondence but some antigens failed to react after transfer because of loss of antigenicity during SDS‐polyacramide gel electrophoresis (SDS‐PAGE). Some antigens were observed preferentially after the transfer procedure, possibly because of their failure to elute from the immunoabsorbant or because they may have a low methionine content. The transfer method failed to reveal the antigen reactivity of three out of four monoclonal antibodies tested, apparently because the epitopes involved were inactivated by SDS. During P. knowlesi infection in the resistant kra monkey (Macaca fascicularis) the transfer method showed the presence by day 10 of antibodies against two components having an apparent molecular weight by SDS‐PAGE similar to those of putative protective antigens described in other studies using monoclonal antibodies.
Serotypic variation of culture‐adapted isolates of P. falciparum
Authors: COWEN N. , CLANCY R. , CRIPPS A. , ALPERS M.
Published: October 2007

Summary Culture adapted isolates of P. falciparum had different growth patterns (P < 0.01) when cultured in the presence of sera obtained from 31 healthy Papua New Guinea residents. Both enhancement and suppression of growth was observed. Less variation was observed using an indirect immunofluorescent antibody method directed against schizont antigens, and no correlation between the two assays was found. This bioassay is assessed as a basis for serotyping P. falciparum strains.
Induction of a protective immune response in rats by injection of live or killed S. mansoni worms
Authors: KNOPF P.M. , SPITALNY K.C. , DANG ANH
Published: October 2007

Summary Resistance to S. mansoni cercarial challenge, induced by prior infection of rats with cercariae, is analysed by substitution of alternatives to the primary cercarial exposure. Intravenous injections of either live or killed 4‐week stage worms have been examined, utilizing two different routes of injection, one or two injected doses, and two different methods to kill worms. In addition to assessing peripheral blood eosinophil levels, anti‐schistosome antibody titres, and challenge worm burdens in the injected and control recipients, sera from these rat groups collected 3 weeks after challenge were used for passive immunization studies in rats. Recipients of intravenous live worm injections were resistant to a cercarial challenge and yielded sera capable of passively immunizing rats. Recipients of intravenous killed worm injections were not significantly resistant to a challenge infection, yet paradoxically, yielded sera capable of passively immunizing rats. Serum from challenge control rats was not significantly protective in the passive immunization assay. There were no correlations between peripheral blood eosinophil levels or anti‐schistosome antibody titres and resistance (either active or passive). We conclude that killed worms induce an immune response which, although insufficient to provide protection by itself, can be recalled or augmented by a challenge infection to result in significant levels of serum protective activity.
Broncho‐alveolar leucocyte responses during primary and secondary Nippostrongylus brasiliensis infection in the rat
Authors: EGWANG T.G. , GAULDIE J. , BEFUS D.
Published: October 2007

Summary Using broncho‐alveolar lavage, we have studied the cellular responses in the rat lung following primary and secondary infection with Nippostrongylus brasiliensis. During the primary infection, there was a biphasic increase in total broncho‐alveolar leucocytes and in the absolute numbers of macrophages, neutrophils, eosinophils and lymphocytes. The first peak occurred on days 4–6, and the second peak occurred around day 16, after infection. During the secondary infection there was an anamnestic‐like response by all cell types. These data suggest that the broncho‐alveolar leucocyte responses to infection have an immunological basis and that in addition to the alveolar macrophage, neutrophils, eosinophils and lymphocytes may play a significant role in lung resistance against migrating helminth larvae.
Chemiluminescence response of peritoneal exudate cells from mice infected with virulent and avirulent strains of Toxoplasma gondii
Authors: MASIHI K.N. , WERNER H. , GILLERT K.‐E. , LANGE W.
Published: October 2007

Summary The zymosan‐triggered chemiluminescence response of peritoneal exudate cells from mice infected with relatively virulent or avirulent Toxoplasma gondii strains was examined at various intervals after infection. Toxoplasma infections increased the background chemiluminescence compared with controls, but higher values were attained earlier in virulent than avirulent infection. A phase of transient unresponsiveness to zymosan was observed with both types of toxoplasma strains. Chemiluminescence continued to decline even after the addition of zymosan on day 3 of infection with the virulent strain but only on day 10 with the avirulent strain. Generation of chemiluminescence was enhanced in mice which had been infected with either strain for 1 month.
Genetic control of susceptibility of mice to infection with E. histolytica
Authors: GHADIRIAN E. , KONGSHAVN P.A.L.
Published: October 2007

Summary Genetic susceptibility to Entamoeba histolytica infection in nine inbred strains and one outbred strain of mice was studied. The number of E. histolytica trophozoites in the ceca of the mice was examined 5 days after intracecal inoculation of axenic amoebae. C3H/HeCr, BALB/c, NZB/BIN, BIO.A, DBA/2 and C57BL/6 were susceptible whereas A/J, CE, DBA/1 and CD‐I mouse strains were relatively resistant. Examination of F1 hybrid animals derived from susceptible B10.A and resistant A/J strains of mice showed that susceptibility was dominant over resistance. Segregation analysis of backcross and F2 progeny derived from the same progenitor strains is compatible with the hypothesis that susceptibility to E. histolytica infection in mice is controlled by a single, dominent gene which has been designated Enh. No association was found between the H‐2 haplotype and the trait of susceptibility to amoebiasis, indicating that the major histocompatibility complex does not play a major role in regulating the early phase of the response to infection with E. histolytica.
Antigen specific and concanavaiin A‐induced lymphocyte blastogenesis responses during the course of Plasmodium berghei infection in rats
Authors: RAYBOURNE R. , DESOWITZ R. S. , SANGHIRUN C.
Published: October 2007

Summary Antigen specific and concanavaiin A (Con A)‐induced lymphocyte blastogenesis responses were monitored in the spleens of rats infected with Plasmodium berghei. Con A responses were depressed only at the time of peak parasitaemia. The antigen specific blastogenesis response was either not in evidence, or at a low level during the periods of patent or subpatent infection (up to 8 weeks after infection). Higher levels of blastogenesis were seen from 8 to 12 weeks after infection, which correlates with clearance of subpatent infection. Fractionation of immune spleen cell suspensions on nylon wool columns indicated that purified T cells did not respond to parasite antigen.
Role of cellular immunity in protection against Trypanosoma cruzi in mice
Authors: TRISCHMANN T. M.
Published: October 2007

Summary The importance of antibodies in the maintenance of immunity against Trypanosoma cruzi in mice is emphasized by the failure of either immunization or transfer of immune T cells to afford B cell suppressed mice complete protection against a lethal infection. Both procedures did, however, significantly prolong survival indicating a contributory role for T cells other than simply as helper cells in antibody production. The complete protection afforded intact mice following transfer of immune T cells can be attributed to a significant T cell‐mediated augmentation of IgG antibody production.
The effect of anti‐malarial drugs on human natural killer cells in vitro
Authors: FERRANTE A. , GOH D. H. B.
Published: October 2007

Summary Human natural killer (NK) cell cytotoxicity against K‐562 target was found to be markedly depressed by quinacrine, mefloquine, pyrimethamine and chloroquine. The most potent were quinacrine and mefloquine. Two other drugs tested, quinine and primaquine, displayed no significant effects even after long incubation periods with effector cells. The results showed that the inhibitory effects were not related to an inhibition of effector cell binding to target or to a toxic effect on NK cells.
Antibody response against schistosomulum surface antigens and protective immunity following immunization with highly irradiated cercariae of Schistosoma mansoni
Authors: SIMPSON A. J. G. , HACKETT F. , WALKER T. , DE ROSSI R. , SMITHERS S. R.
Published: October 2007

Summary The production of antibodies against the schistosomulum surface antigens of Schistosoma mansoni in response to immunization with highly irradiated cercariae was followed. Four antigens were reproducibly identified by 125I surface labelling using lodogen and immunoprecipitation; they had mol. wts of 38, 32, 20 and 15 kD. In addition a 92 kD antigen was also evident in most experiments. It was demonstrated that the 20 kD antigen was the same as that recognized by the monoclonal antibody NIMP/M.47 and that this antigen like the 38 and 32 kD antigens was thus identified during both chronic infection and following vaccination with irradiated cercariae. Two weeks following immunization with irradiated cercariae antibody was produced only against the 15 kD antigen but at 4 weeks the major response was against the 32 kD antigen. A second immunization with irradiated cercariae boosts the antibody response so that all four antigens were strongly precipitated. Further vaccinations did not lead to the identification of further antigens. Immunization of rats with highly irradiated cercariae also resulted in antibody production against the 38, 32, 20 and 15 kD antigens. Surface labelling of schistosomula transformed from irradiated cercariae resulted in the same four antigens being precipitated as from normal cercariae indicating that irradiation did not affect transformation nor antigen expression on 3h schistosomula. Furthermore, antibodies againt the same surface antigens were detectable 4 weeks after immunization with equal numbers of cercariae irradiated with 0, 5, 25 or 50 krad. Vaccination of mice with irradiated, cloned cercariae resulted in identical antibody production and similar levels of immunity directed at both an homologous or heterogeneous challenge. Thus all parasites within our laboratory population appear to express the same antigens and there was no evidence for a genetically defined variation that could account for the
Genetic control of immunity to Nematospiroides dubius: a 9‐day anthelmintic abbreviated immunizing regime which separates weak and strong responder strains of mice
Authors: BEHNKE J. M. , ROBINSON M.
Published: October 2007

Summary Experiments were designed to re‐examine the variables which influence the ability of single primary infections to elicit acquired immunity to Nematospiroides dubius, in particular the importance of the presence or absence of adult worms, as these are known to exert immunomodulatory effects. Briefly, anthelmintic abbreviated infections were considerably more effective at eliciting acquired immunity than longer infections in which adult worms were allowed to reside in the intestine. A 9‐day anthelmintic abbreviated infection was extremely effective at stimulation of acquired immunity in NIH mice and very few immunising infection larvae were required. Immunity to subsequent reinfection developed rapidly after the primary infection worms had been eliminated; by day 21 post‐infection, the mice were almost totally immune. Abbreviated infections were used to examine the capacity of a number of mouse strains to develop immunity to reinfection. Strains of mice were chosen to allow the effects of MHC linked and non‐MHC linked (background) genes to be identified. CBA and C3H strains (both H‐2k) were found to be weak responders to N. dubius. B10G (H‐2q) mice responded better than C57B1/10 (H‐2b), although these strains have identical background genes. DBA/2 mice were stronger responders compared to BALB/c mice, both strains sharing a common MHC haplotype (H‐2d). (NIH × B10G) F1 mice (H‐2q) were better responders than either of the parental strains. Several mouse strains all sharing the H‐2q haplotype were particularly effective at developing immunity to N. dubius, as were also SJL mice which were the sole representatives of the H‐2s haplotype, in the present study. The results established that the response phenotype is influenced by both background and MHC genes and demonstrated gene complementation in the capacity of mice to acquire immunity to N. dubius.
Cellular and humoral inhibition of Plasmodium falciparum growth in vitro and recovery from acute malaria
Authors: BROWN J. , GREENWOOD B. M.
Published: October 2007

Summary Both mononuclear cell cytotoxicity and serum inhibition of Plasmodium falciparum growth in vitro were found to vary according to the stage of infection in Gambian children with clinical malaria. Cytotoxicity was displayed by mononuclear cells and serum from children with acute malaria but this form of parasite killing was more effective in children with low grade P. falciparum infections of at least 10 days duration. Parasite inhibitory antibody was not evident in sera from acutely infected children but was found in sera from children recovering from malaria and reached a peak in convalescent children when P. falciparum growth was inhibited by at least 50%. The humoral response in convalescent children was strain related, being more effective against the most recent infecting parasite strain than against other ‘wild’P. falciparum isolates. In contrast, mononuclear cell cytotoxicity was not strain related; when effective, multiplication of all parasite isolates tested was retarded to the same degree. The discussion considers the role of mononuclear cell cytotoxicity in the development of protective immunity and suggests that it may be a ‘front line’ defense mechanism during each malaria attack.
Ultrastructural studies of the killing of schistosomula of Schistosoma mansoni by activated macrophages in vitro
Authors: McLAREN DIANE J. , JAMES STEPHANIE L.
Published: October 2007

Summary Immunologically activated murine macrophages have been shown elsewhere to kill skin stage schistosomula of Schistosoma mansoni in vitro, in a manner analogous to the extracellular killing of tumour cell targets. In this study, the kinetics of the interaction between activated macrophages and larval targets and the resultant ultrastructural changes in parasite morphology that culminated in death have been analysed in detail. Unlike granulocyte‐mediated schistosomular killing, macrophage‐mediated cytotoxicity did not appear to be directed against the surface tissues of the parasite. Macrophages adhered only transiently following initiation of the cultures, yet changes in the subtegumental mitochondria and muscle cells of the larva were detected within the first hour of incubation. Progressive internal disorganisation followed rapidly, but the tegument and tegumental outer membrane remained intact, to form a ‘shell’ that maintained the general shape of the parasite. Such changes were recognised irrespective of whether the effector cell population comprised peritoneal macrophages activated by lymphokine treatment in vitro, or by infection with Mycobacterium bovis (strain BCG), or S. mansoni in vivo. That macrophages rather than contaminating granulocytes or lymphocytes, had mediated the observed damage was demonstrated by the use of a lymphokine treated macrophage cell line, IC‐21. The observation that macrophage cytotoxicity is directed against internal organelles rather than the tegumental outer membrane of this multicellular target, may help to elucidate the general mechanism of extracellular killing by these cells.
Inhibition of human monocyte locomotion by products of axenically grown E. histolytica
Authors: KRETSCHMER R. , COLLADO M. L. , PACHECO M. G. , SALINAS M. C. , LÓPEZ‐OSUNA M. , LECUONA M. , CASTRO E. M. , ARELLANO J.
Published: October 2007

Summary The supernatant fluid of axenically grown E. histolytica inhibits chemotaxis, chemokinesis and random mobility of human mononuclear phagocytes (MP) as measured in Boyden chambers. Human polymorphonuclear phagocytes (PMN) locomotion is apparently unaffected. The factor was found in comparable amounts in the supernatant fluid of axenic cultures of four E. histolytica strains that differed in their human pathogenicity and virulence, as well as in two entamoebas non‐pathogenic for man. This dialysable and thermolabile MP‐locomotion inhibiting entamoeba product (EP) can be absorbed out by incubation with MP, but not with lymphocytes, while partial absorption was observed using PMN. The MP‐locomotion inhibitory effect of this EP was cancelled by inhibiting protein synthesis in the MP by means of cycloheximide. In vivo, this EP caused a delay in MP migration in Rebuck skin windows. The molecular weight of this EP lies between 478 and 765 by gel‐sieve chromatography. Our results suggest a direct effect upon the cytoskeletal and locomotive apparatus of the MP. This MP‐locomotion inhibiting EP could contribute to the paucity of the inflammatory reaction observed in the advanced stages of invasive amoebiasis and consequently also to the lack of scar tissue formation upon healing of amoebic lesions.
Susceptibility to coccidiosis: contrasting course of primary infections with Eimeria vermiformis in BALB/c and C57/BL/6 mice is based on immune responses
Authors: ELAINE ROSE M. , WAKELIN D. , HESKETH PATRICIA
Published: October 2007

Summary The effects of three immunosuppressive treatments‐whole body irradiation and injections of cortisone acetate or cyclophosphamide, on the course of primary infections with Eirneria verniformis were investigated in ‘resistant’ BALB/c and ‘susceptible’ CS7BL/6 mice. Immunosuppression (and the nude athymic mutation in BALB/c mice) resulted in increased reproduction of the parasite in both strains of mice, indicating some immunological control of primary infections. The effect was, however, very much more marked in the BALB/c mice, resulting in an alteration in the relative susceptibilities of the two strains. The findings are discussed and it is suggested that the basis for the differences observed in the course of infection in normal BALB/c and C57BL/6 mice lies in their immune responses to this parasite.
Invasion of erythrocytes in vitro by Plasmodium falciparum can be inhibited by monoclonal antibody directed against an S antigen
Authors: SAUL A. , COOPER J. , INGRAM L. , ANDERS R. F. , BROWN G. V.
Published: October 2007

Summary A monoclonal antibody has been produced which binds to the heat stable S antigen present in the FCQ‐27/PNG isolate of Plasmodium falciparum. This monoclonal antibody also inhibits the invasion in vitro of erythrocytes by malarial merozoites thus demonstrating that the S antigens of Plasmodium falciparum may be a target of protective immune responses.
Monoclonal anti‐gamete antibodies prevent transmission of murine malaria
Authors: HARTE P. G. , ROGERS N. C. , TARGETT G. A. T.
Published: October 2007

Summary Three monoclonal antibodies prepared using spleen cells from mice immunized with microgametes of Plasmodium yoelii nigeriensis were tested for their ability to block transmission of the infection. Two of them agglutinated microgametes and blocked transmission, this effect being antibody‐dose dependent. The third monoclonal used alone was ineffective in both these assays although it stained gametocytes and microgametes by immunofluorescence in the same way as the protective monoclonals. However, when it was administered in combination with one of the protective monoclonals the transmission blocking immunity was enhanced significantly, indicating a synergistic effect of the two antibodies.
Serum dependent cell‐mediated immune reactions to Brugia pahangi infective larvae*
Authors: CHANDRASHEKAR R. , RAO U. R. , SUBRAHMANYAM D.
Published: October 2007

Summary Fresh normal rat serum (fNRS) promoted adherence and cytotoxicity of albino rat neutrophils and macrophages to Brugia pahangi infective larvae (L3) in vitro. EDTA and not EGTA abolished the adherence activity suggesting the involvement of complement components via the alternate pathway. C3 molecules were detected on the surface of the parasite by immunofluorescence. fNRS depleted of complement by treatment with Zymosan A or of factor B by heating at 50°C for 20 min, failed to promote cell adherence to the parasite. fNRS and cells from albino rat were more potent in inducing cytotoxicity to L3 than those from jird or Mastomys which may reflect the greater resistance offered by the albino rat to B. pahangi infection. In the presence of IgG and a heat labile factor, possibly complement, of immune serum, neutrophils and macrophages and to a lesser extent eosinophils adhered to and killed the larvae. Immune sera raised against microfilariae of different filarial parasites promoted cell‐mediated cytotoxicity to B. pahangi L3 suggesting sharing of antigens between the two stages.
Effects of host serum on feeding by Trichostrongylus colubriformis (nematoda)
Authors: BOTTJER K. P. , KLESIUS P. H. , BONE L. W.
Published: October 2007

Summary The effect of host serum on in vitro feeding by Trichostrongylus colubriformis was studied by incubating adult helminths in goat serum containing the dye, Rhodamine B. The amount of dye ingested was determined by fluorometric analysis. Immune serum from goats infected with T. colubriformis suppressed helminth feeding, while normal serum from uninfected goats did not. Suppression of feeding by immune serum increased with the duration of the host's infection. Heat‐inactivation (56°C) of immune serum did not affect its suppressive activity. Pre‐exposure of worms to immune serum decreased subsequent feeding activity. However, rigorous washing of helminths restored their feeding to levels that were similar to untreated worms. Indirect immunofluorescent studies with immune serum and FITC conjugated rabbit anti‐goat IgG demonstrated binding of immunoglobulin to the cuticle, stoma and excretory pore of whole worms. Feeding inhibition of immune serum was associated with IgG1 isotype. Results of the present studies indicated that IgG was responsible for in vitro suppression of T. colubriformis feeding and may be one effector of immunity to T. colubriformis in the goat.
The role of the macrophage in immunity to Trypanosoma musculi
Authors: FERRANTE A.
Published: October 2007

Summary Trypanosoma musculi was killed by adherent peritoneal exudate cells which had the typical appearance of macrophages. Observations by light and electron microscopy showed that the trypanosomes were phagocytozed and killed intracellular^ within phagocytic vacuoles of mouse macrophages. Adherence, phagocytosis and killing of T. musculi required the presence of serum from mice immune to this parasite. Phagocytosis and killing of T. musculi was highly dependent on heat‐labile factors in immune mouse serum.
M. Leprae phagocytosis and its association with membrane changes in macrophages from leprosy patients
Authors: MISTRY N. F. , BIRDI T. J. , ANTIA N. H.
Published: October 2007

Summary Abnormal phagocytosis of Mycobacterium leprae by macrophages of lepromatous patients was demonstrated under various conditions. The largest proportion of macrophages with an excessive bacterial load belonged to the lepromatous group of patients. Lepromatous macrophages treated with Cytocha‐lasin B, an inhibitor of phagocytosis, exhibited a significantly lower degree of ingestion of heat‐killed organisms whereas uptake of ‘viable’ organisms was not affected to the same extent. Regulation of phagocytosis was studied by noting the rate of phagocytosis of M. leprae after the ingestion of a primary particle viz carbonyl iron. Solely in lepromatous macrophages, phagocytosis of carbonyl iron did not result in a decreased uptake of M. leprae implying aberrant phagocytic activity. Lastly, excessive phagocytosis was always noted in macrophages of familial contacts of leprosy patients who displayed decreased Fc receptor expression after M. leprae ingestion. This is of interest since phagocytosis, like Fc receptor expression, is a membrane dependent event and other membrane associated defects have been recognized by us earlier in lepromatous macrophages.
Specific lysis ofTheileria annulata‐infectedlymphoblastoid cells by a monoclonal antibody recognizing an infection‐associated antigen
Authors: PRESTON PATRICIA M. , MCDOUGALL CATHIE , WILKIE GWEN , SHIELS B. R. , TAIT A. , BROWNf C. G. D.
Published: October 2007

SummaryA monoclonal antibody (4H5) recognizing aTheileria annulatainfection‐associated antigen was assayed to see if it could either suppress the proliferation ofT. annulata‐infectedlymphoblastoid cells, as monitored by the incorporation of triated thymidine by proliferating host cells, or lyseT. annulata‐infectedlymphoblastoid cells, as assessed by counts of target cell numbers and examination of Giemsa stained smears. These assays showed that binding of the monoclonal antibody, in the presence of complement, both lysed and suppressed the proliferation of theT. annulataHissar‐infected cell line against which this monoclonal antibody was raised. This effect extended both to other (allogeneic)T. annulataHissar‐infected cell lines and to lymphoblastoid cell lines infected with other geographical stocks ofT. annulata.An uninfected bovine lymphoid cell line was not affected by the antibody. The results obtained in thesein vitroexperiments are taken to mean that binding of the monoclonal antibody 4H5 to aT. annulatainfection‐associated antigen, in the presence of complement, will lyse and suppress specifically the proliferation ofT. annulata‐infectedlymphoblastoid cells. These observations raise the possibility that immunization of cattle with the purifiedT. annulatainfection‐associated antigen recognized by this monoclonal antibody may provoke immune responses which are capable of suppressing the proliferation ofT. annulata‐infectedlymphoblastoid cellsin vivoand thus provide an effective method of immunoprophylaxis against tropical theileriosis.
Immune responses to eimeria: quantification of antibody isotypes to Eimeria tenella in chicken serum and bile by means of the ELISA
Authors: MOCKETT A. P. ADRIAN , ROSE M. ELAINE
Published: October 2007

Summary The enzyme‐linked immunosorbent assay (ELISA) has been used to study the serum IgM and IgG response and the bile IgA and IgM response of chickens to a primary, secondary and tertiary inoculation of Eimeria tenella. In the serum there was a rapid and transient IgM response to the primary infection; second and third inoculations of oocysts had comparatively little effect on the concentrations of this antibody isotype. This differed from the specific IgG response which was later and of similar magnitude after each inoculum. In the bile, specific IgA reached its highest concentrations 9–10 days after the primary inoculation and then declined rapidly. The second and third inoculations each induced low concentrations of this isotype. The specific biliary IgM response to the primary inoculation was similar in profile to that of the IgA, but IgM was detected only on day 14–15 after the second and not at all after the third inoculation. The findings are discussed and are compared with the results obtained using other host species, principally the rat, and with other gut organisms. The relevance of the antibody response in resistance to eimerian infections is also discussed.
Immunoglobulin class responses to Taenia taeniaeformis in susceptible and resistant mice
Authors: GIBBENS J. C. , HARRISON L. J. S. , PARKHOUSE R. M. E.
Published: October 2007

Summary The immunoglobulin class response of two inbred strains of mice, C57BL/6 and C3H/He, to infection and challenge with Taenia taeniaeformis larvae was compared using the enzyme‐linked immunosorbent assay and gel electrophoresis followed by immunoelectrotransfer blot (Western blotting) techniques. The C57BL/6 mice, which are relatively resistant to infection, had a more restricted humoral response than the more susceptible, C3H/He mice. C3H/He mice produced a wider range of immunoglobulin classes, in particular IgA and IgG3, to those antigens recognized by both strains of mice. In addition they produced antibodies to a wider range of antigens. The production of these additional antibodies by the susceptible strain raises the possibility that some of the antibodies may have specificities which interfere, or block the action of potentially protective antibodies. Antibodies, mainly of the IgG1, IgG2a and IgG2b classes, to antigens of approximately < 21000, 21000–23000, 30000 and 60000 mol. wt, present both in the oncosphere and the metacestode extracts, were found in serum from previously infected and resistant mice of both strains. These antigens may be important in stimulating protective concomitant immunity.
Genetic influence on the antibody response to antigens of Schistosoma mansoni in chronically infected mice
Authors: KEE KIRK C. , TAYLOR DAVID W. , CORDINGLEY JOHN S. , BUTTERWORTH ANTHONY E. , MUNRO ALAN J.
Published: October 2007

Summary Immunoprecipitations of in vitro translation products of mRNA from adult Schistosoma mansoni worms with sera from chronically infected mice of 12 inbred strains reveal a strain‐dependent heterogeneity in the antibody responses to schistosome antigens. Of the strains tested the response to the 86K antigen was restricted to mice of haplotypes H‐2d H‐2k, and H‐2k while the 14K antigen was only recognized by H‐2k mice. Responses to other antigens revealed the influence of non‐H‐2 genes on the antibody response although no clear correlation was apparent between the antigens recognized and the non‐H‐2 genes of the strains. Both dominant and recessive responses towards individual antigens were seen in F| animals. Some of these results support the cross tolerance model of Ir gene function.
Schistosoma mansoni egg antigens: preparation of rabbit antisera with monospecific immunoprecipitating activity, and their use in antigen characterization
Authors: DUNNE D. W. , AGNEW ALISON M. , MODHA J. , DOENHOFF M. J.
Published: October 2007

Summary A simple method for producing monospecific rabbit antisera, applied originally to the constituents of human serum (Goudie et al. 1966), has been adapted for use with Schistosoma mansoni egg antigens. Replicate isolated immunoprecipitin arcs resulting from the immunoelectrophoretic reaction between an egg antigen and a polyspecifk antiserum were excised, washed extensively to remove non‐precipitated contaminants, homogenized, and emulsified with complete Freund's adjuvant. Rabbits were given weekly subcutaneous injections of the emulsion in multiple sites, and a monospecific precipitating antibody against the respective immunizing antigen generally resulted within 6 weeks of the commencment of immunization. Antisera raised in this manner against S. mansoni egg antigens tui, oti and Ks have been used to characterize the antigen with respect to their stage‐ and species‐specificity. After immunoabsorp‐tion to remove background activity, the sera could be used to detect unequivocally the respective antigens in crude egg homogenate that had been subjected to SDS‐PAGE and electrotransfer to nitrocellulose paper.
Spleen and lymph node cell populations, In vitro cell proliferation and interferon‐y production during the primary immune response to Toxoplasma gondii
Authors: JONES THOMAS C. , ALKAN SEFIK , ERB PETER
Published: October 2007

Summary An animal model for the study of transient lymphadenopathy‐splenomegaly during toxoplasmosis is presented. Injection of CBA/J mice with the low virulent, cyst‐forming strain of Toxoplasma gondii (Pe strain) induces a three to four fold increase in weight and cellularity of spleen and lymph nodes with peak changes at 30–50 days after infection. The spleen displays marked haemopoiesis, a 30 fold increase in mononuclear phagocytes, and a two fold increase in Lyt2+ lymphocytes. Lymph nodes show a five fold increase in mononuclear phagocytes and a four and a half fold increase in Lyt2+ T cells. The increase in mononuclear phagocytes significantly alters T cell/macrophage ratios and this is associated with decreases in in vitro cell proliferation to mitogen and toxoplasma antigen. The relationship between alterations in cell balance of mononuclear phagocytes and T cell subsets and the expression of transient immune dysfunction can now be examined by modulating changes in these cell types.
Active suppression of interleukin 2 secretion in mice infected with Trypanosoma brucei AnTat 1.1. E
Authors: SILEGHEM MAARTEN , HAMERS RAYMOND , BAETSELIER PATRICK DE
Published: October 2007

Summary Impairment of T cell proliferation in mice infected with the pleomorphic Trypanosoma brucei AnTat LIE clone was found not to be related to a depletion of T cells or to an absence of functional accessory cells, but rather to an active suppression of interleukin 2 (IL‐2) production. Lymph node cells derived from infected mice failed to produce IL‐2 following Con A stimulation, whereas an exogenous supply of recombinant IL‐2 could restore the impairment of the mitogen (Con A)‐induced proliferative responses. Furthermore, lymph node cells derived from infected mice suppressed both secondary T‐cell proliferative responses and IL‐2 secretion, indicating that the trypanosome‐induced suppression is mediated by a suppressive cell which interferes at the level of IL‐2 secretion.
Specific suppression of delayed hypersensitivity expression to Trypanosoma cruzi in mice
Authors: HELOISA M. , BLOTTA S. L. , CUROTTO M. ALICIA , ABRAHAMSOHN ISES A.
Published: October 2007

Summary The absence of cutaneous delayed type hypersensitivity (DTH) expression was investigated in Trypanosoma cruzi infected mice. Neither spleen cells nor peritoneal exudate cells from infected mice transferred DTH to normal recipients in local or systemic adoptive transfer experiments. Expression of DTH in T. cruzi immunized mice was suppressed specifically by Thy‐1 negative spleen cells from acutely and subacutely infected animals. Suppression was observed only upon systemic transfer, but not when infected mice spleen cells were added to DTH effector cells and transferred to normal recipients. These results suggest that cutaneous DTH expression in acutely infected mice, might be blocked by mechanisms other than those described for suppression of lymphocyte proliferation and of DTH induction to T. cruzi.
Effect of protective and non‐protective antibodies in the phagocytosis rate of Trypanosoma cruzi blood forms by mouse peritoneal macrophages
Authors: LAGES‐SILVA ELIANE , RAMIREZ LUIS E. , KRETTLI ANTONIANA U. , BRENER Z.
Published: October 2007

Summary The phagocytosis of Trypanosoma cruzi blood forms by mouse peritoneal macrophages is significantly enhanced by sera from chronic chagasic patients, rabbits and mice presenting ‘lytic antibodies’ (LA) which are associated with resistance and active infections as well as ‘conventional serology antibodies’ (CSA) which are immunoglobulins involved in the positivity of serological diagnostic tests. The phagocytosis rate, however, is not influenced by sera from mice immunized with T. cruzi antigen or chagasic patients submitted to specific treatment, both displaying only CSA but not LA. The efficacy of LA in increasing phagocytosis is related to their ability to bind to epitopes of living trypomastigotes, a property lacking in CSA that bind only to fixed parasites. This phenomenon is apparently the reason for the low effectiveness of antigens used for vaccination in Chagas' disease which only induce CSA, immunoglobulins apparently unable to mediate a number of regular effector immune mechanisms such as complement‐mediated lysis, antibody‐dependent cell cytotoxicity and phagocytosis.
Isolation of an antigenic fraction for diagnosis of Onchocerciasis
Authors: CABRERA Z. , PARKHOUSE R. M. E.
Published: October 2007

Summary A surface enriched fraction was prepared from adults of Onchocerca volvulus by brief extraction of entire worms with detergent. This was then gel filtered to yield a low molecular weight fraction which functioned specifically in ELISA analysis. An identical result was also obtained when the related cattle parasite, O. gibsoni, was similarly fractionated and tested. The low molecular weight fraction contained at least four antigenic components when examined by coprecipitation and immunoblotting studies. One ml of packed worms yielded sufficient low molecular weight antigen to examine about 2000 human sera by the ELISA procedure, and the test was sensitive at human serum dilutions down to 1/400. A preliminary study with individual sera from Onchocerciasis endemic and non‐endemic areas of Southern Mexico yielded 0/24 false positives, 3/24 false negatives and a significant ELISA value in 21/24 sera from proven cases of Onchocerciasis.
Immune complex glomerulonephritis in experimental kala‐azar
Authors: SARTORI ALEXANDRINA , DE OLIVEIRA ALBANITA VIANA , ROQUE‐BARREIRA MARIA CRISTINA , ROSSI M. A. , CAMPOS‐NETO A.
Published: October 2007

Summary In the present work we demonstrate that hamsters infected with L. donovani eliminate large quantities of immunoglobulins in the urine. This alteration is clearly a consequence of a conspicuous immune complex glomerulonephritis readily detectable 7 days after the beginning of infection. L. donovani antigens and hamsters immunoglobulins (Igs) were revealed as granular deposits in the mesangial areas and contiguous loops of the glomeruli.

Histopathological alterations such as focal mesangial proliferation with progression to diffuse proliferation were observed in the first 3 weeks of infection. From day 35 onwards, all diseased animals presented large deposits of amyloid material of predominantly glomerular localization.

In consonance with these alterations, Igs were detected in the urine by day 21 of infection and their concentration increased substantially with the progression of disease. In contrast, serum Igs increased until day 21, when their concentration dropped steadily.
Suppression of muscosal mastocytosis by infection with the intestinal nematode Nematospiroides dubius
Authors: DEHLAWI M. S. , WAKELIN D. , BEHNKE J. M.
Published: October 2007

Summary Mice exposed to primary infections with the parasitic intestinal nematode Nematospiroides dubius failed to show the mucosal mast cell (MMC) response which is characteristic of infections with other species of intestinal nematode and which was readily induced in these mice by infections with Nippostrongylus brasiliensis or Trichinella spiralis. The failure to generate a mucosal mastocytosis was independent of host strain or sex. When infections with N. dubius were established before, or concurrently with, T. spiralis or N. brasiliensis, the MMC response elicited by these species was delayed and/or depressed as was expulsion of the worms themselves. Infection with N. dubius given when a MMC response was already established, by exposure to T. spiralis, had no effect on MMC numbers. The possibility that the effects of N. dubius upon MMC responses reflect a lack of mastocytopoietic potential, rather than an active interference, was excluded by showing that SJL mice, which expel primary infections with N. dubius and express strong immunity to reinfection, developed marked mastocytosis during secondary infections. The depression of MMC responses by N. dubius is discussed in relation to the known immunosuppressive properties of this parasite and in relation to the T cell mediated control of MMC development.
Inhibition of equine neutrophil chemotaxis and chemokinesis by a Taenia taeniaeformis proteinase inhibitor, taeniaestatin
Authors: LEID R. W. , GRANT R. F. , SUQUET CHRISTINE M.
Published: October 2007

Summary Taeniaestatin, a recently isolated Taenia taeniaeformis proteinase inhibitor, was used to inhibit equine neutrophil migration. Taeniaestatin itself was not chemotactic when used as a chemotactic factor but taeniaestatin did inhibit neutrophil chemokinesis when tested in a Zigmond‐Hirsch checkerboard assay. A dose‐dependent inhibition of both chemokinesis and chemotaxis was observed when zymosan activated bovine sera (ZABS) was used as the chemotactic factor. This inhibition was > 95% when 5 u of taeniaestatin was present on both the cell and chemotactic factor side of the chambers. Equine neutrophils gave dose‐ and time‐dependent migration responses to purified bovine C5a with an ED50 of 1±04 ± 10–7 M. Taeniaestatin inhibited the C5a‐mediated chemotactic and chemokinetic neutrophil responses (51% using 1 u and > 95% with 5 u of taeniaestatin). The inhibition of leucocyte motility by taeniaestatin was reversible and without cytotoxicity at the highest doses of taeniaestatin tested.
The virulence of Trypanosoma congolense can be determined by the antibody response of inbred strains of mice
Authors: ROELANTS G. E. , PINDER M.
Published: October 2007

Summary Three inbred strains of mice, BALB/c, C57B1/6 and CBA J were infected with three clones of Trypanosoma congolense, DIND/3–1, SAM 28±1 and KAR/57±1, which were obtained from three different stocks. DIND/3±1 was of high virulence for BALB/c and CBA/J but of negligible virulence for C57B1/6. SAM/28±1 was of high virulence and KAR/57±1 of negligible virulence for the three strains of mice. In each case, high virulence was correlated with a late, transient and low titre protective antibody response measured by complement mediated lysis of live organisms. Negligible virulence was correlated with an early, high titre protective antibody response. Suppression of the antibody response by sub‐lethal irradiation or cyclophosphamide treatment of the host turned a trypanosome infection of negligible virulence into one of high virulence. In mice with mixed infections it was shown that highly virulent trypanosomes did not influence the course of infection and antibody response to trypanosomes of negligible virulence and vice‐versa. The relationship of total antigen mass to the kineties of the antibody response suggests that 1000‐ to 10000‐fold less antigen is required in good responder than in bad responder mice to trigger the immune response. Thus the virulence of T. congolense can be determined by the antibody response of inbred strains of mice. The specificity and dose dependency of this antibody response seem to implicate the involvement of Ir genes.
Isolation and characterization of a monoclonal anti‐P30 antibody resistant mutant of Toxoplasma gondii
Authors: KASPER LLOYD H.
Published: October 2007

Summary Of the possible iodine‐labelled Toxoplasma gondii surface proteins, P30 (apparent Mr 30000) is the principal one recognized by acute and convalescent anti‐toxoplasma sera. This protein which comprises from 3 to 5% of the total parasite protein was used to raise a panel of parasiticidal monoclonal anti‐P30 antibodies. One of these monoclonal antibodies was able to select a resistant mutant from a large population of chemically mutagenized wild‐type P strain parasites. This mutant retained the wild type sensitivity to other non‐P30 parasiticidal monoclonal antibodies as well as polyclonal anti‐P30 rabbit sera. Analysis of surface radioiodinated wild type and mutant parasites showed that the mutant had a quantitative reduction in the amount of P30. A comparison of surface biotin labelled wild type and resistant parasites by two dimensional electrophoresis showed that the mutant lacked one and possibly two of several proteins that make up wild type P30. Western blot analysis indicated that the mutant was devoid of antigenically reactive P30. These findings further support the hypothesis that antigenic variants of T. gondii can be induced and may involve the major surface membrane antigens of the parasite.
Initial induction of immunity, followed by suppression of responses to parasite antigens during Trypanosoma cruzi infection of mice
Authors: TARLETON RICK L. , SCOTT DAVID W.
Published: October 2007

Summary Infection of a relatively resistant strain of mice (C57BL/6J) with the protozoan parasite Trypanosoma cruzi results in both the induction of parasite‐specific T‐helper cells and nonspecific suppressor cells. A time course study of the activation of help and suppression revealed that parasite‐specific T‐helper cell activity increases very early in infection (< 12 days) at a time when suppression of non‐parasite‐specific responses and suppressor cell activity is increasing. Between 12 and 14 days of infection, the T‐helper cell response to T. cruzi, as measured by the antibody response to hapten‐T. cruzi in vitro, is suddenly and dramatically regulated. As reported previously, plastic and G‐10 adherent cells appear to be responsible for the regulation of antibody responses to heterologous antigen during T. cruzi infection. These adherent suppressor cells are also responsible for the suppression of antibody responses to hapten‐T. cruzi following the first 2 weeks of infection. Suppressor cells continue to regulate the parasite‐specific response well into chronic infection even though the response to hapten‐T. cruzi appears to return to normal levels. These results are the first to directly implicate nonspecific suppressor cells in the regulation of anti‐T. cruzi humoral immune responses.