bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibodies directed against nerve growth factor inhibit the acute bronchoconstriction due to allergen challenge in guinea‐pigs
Authors: De Vries A. , Engels F. , Henricks P. A. J. , Leusink‐Muis T. , Fischer A. , Nijkamp F. P. 
Published: March 2003

BackgroundWe have previously demonstrated that the administration of nerve growth factor (NGF) to guinea‐pigs results in airway hyper‐responsiveness within 1 h.Objective In the present study we document the involvement of NGF in the acute allergic airway response.Methods Guinea‐pigs that are sensitized to ovalbumin show an acute bronchoconstriction directly after challenge with ovalbumin.Results Intratracheal application of 10 µg of antibodies directed against NGF (anti‐NGF) 1 h before the challenge reduces the acute severe bronchoconstriction to approximately 40% and the sustained bronchoconstriction to approximately 20% of the reaction in controls. This shows a high potency of anti‐NGF in diminishing the direct bronchoconstriction. Inhibition of the tyrosine kinases of the tyrosine kinase receptor A, the high‐affinity receptor for NGF, has no effect on the bronchoconstriction. Therefore, we postulate that the p75, the low‐affinity receptor for neurotrophins, is responsible for the acute bronchoconstriction. Our findings suggest a role for NGF in the induction of the acute asthmatic reaction.Conclusion These findings offer a new potential therapeutic strategy for the treatment of allergic asthma.
Coding single nucleotide polymorphism in the high‐affinity immunoglobulin E receptor b chain (Fc"RI‐b) gene is associated with immunoglobulin E receptor‐mediated histamine release from basophils
Authors: Kim Y.‐K. , Oh S.‐Y. , Oh H.‐B. , Chun S.‐Y. , Cho S.‐H. , Koh Y.‐Y. , Min K.‐U. , Kim Y.‐Y. 
Published: March 2003

SummaryBackground  Our previous work on linkage analysis showed that histamine release from basophils to anti‐IgE stimuli was linked to the gene marker of chromosome 11q13, where the β chain of the high‐affinity receptor for IgE (FcεRI‐β) is located.Objective  To evaluate the association between FcεRI‐mediated histamine release from basophils and four bi‐allelic single nucleotide polymorphisms of the FcεRI‐β gene.Methods  Phenotypes of asthma, such as maximal histamine release from basophils and atopy, were measured from 80 randomly recruited asthmatic children. Polymorphisms of the FcεRI‐β gene were determined by PCR‐based methods.Results  The polymorphism in exon 7, resulting in Glu to Gly substitution, was significantly associated with histamine release from basophils to anti‐IgE stimuli, but not with total IgE levels and skin test responses to aeroallergens.Conclusion This study supports a role for the FcεRI‐β gene in the expression of high affinity IgE receptor‐mediated histamine release from basophils.
Atopic sensitization among children in an Arctic environment
Authors: Krause T. G. , Koch A. , Poulsen L. K. , Kristensen B. , Olsen O. R. , Melbye M. 
Published: March 2003

Background Asthma has been reported to be rare among Inuits, but so far total and specific IgE levels have never been determined in arctic populations.Objective To determine the prevalence of atopy in children living in an arctic environment, and to examine whether atopy and total IgE levels were associated with parental place of birth, as a measure of ethnicity, and travel history.Material and Methods All schoolchildren in Sisimiut, a community on the West coast of Greenland, were screened for atopy. Blood samples were analysed for total IgE and for specific IgE against inhalant and food allergens. Information on place of birth of children and their parents was obtained from national registries. Information on travel history was obtained from self‐administered questionnaires.Results A total of 1031 schoolchildren aged 5 to 18 years had a blood sample drawn (85% of available children for the study). Of these, 151 (14.6%) children were sensitized to at least one inhalant allergen and 42 (4.1%) to at least one food allergen. Sensitization to grass was most common, whereas sensitization to mugwort, birch, animal‐dander and house‐dust mite was infrequent. Children whose parents were both born abroad had a higher risk of sensitization to inhalant allergens compared with children born of Greenlandic parents (OR = 8.6, 95% CI 2.8–27.1). Furthermore, children who had been abroad had a higher risk of sensitization towards pollen (OR = 1.6, 95% CI 1.0–2.5) and animal‐dander (OR = 2.1, 95% CI 1.0–4.6) after adjustment for confounders. Both atopic and non‐atopic children demonstrated high levels of total IgE (medians of 251 and 58 kU/L).Conclusions Compared with European findings Greenlandic children have high levels of total IgE but a low prevalence of allergic sensitization towards inhalant allergens. This may be due to a low genetic susceptibility to atopy and less allergen exposure, as well as to living conditions in an arctic environment.
Effect of ozone exposure on allergic sensitization and airway inflammation induced by dendritic cells
Authors: Depuydt P. O. , Lambrecht B. N. , Joos G. F. , Pauwels R. A. 
Published: March 2003

Background Epidemiological studies suggest that ozone exposure is related to increased asthma symptoms. Dendritic cells (DCs) are the principal antigen‐presenting cells in the airways.Objective We have examined whether ambient doses of ozone (100 ppb for 2 h) enhance allergic sensitization and/or airway inflammation in a mouse model.Methods C57BL/6 mice were sensitized to inhaled ovalbumin (OVA) by intratracheal instillation of OVA‐pulsed DCs on day 0. Daily exposure to OVA aerosol on days 14–20 resulted in an eosinophilic airway inflammation, as reflected in bronchoalveolar lavage fluid and lung histology. In a first experiment, mice were exposed to ozone or room air immediately prior to and following sensitization. Subsequently, we tested the effect of ozone exposure during antigen challenge in DC‐sensitized mice.Results Exposure to ozone during sensitization did not influence airway inflammation after subsequent allergen challenge. In contrast, in sensitized mice, challenge with OVA together with ozone (days 14–20) resulted in enhanced airway eosinophilia and lymphocytosis, as compared with mice exposed to OVA and room air (1.91 × 106 ± 0.46 × 106 vs. 0.16 × 106 ± 0.06 × 106 eosinophils/mL lavage fluid; P = 0.015; 0.49 × 106 ± 0.11 × 106 vs. 0.08 × 106 ± 0.03 × 106 lymphocytes/mL lavage fluid; P = 0.004). Ozone exposure without subsequent OVA exposure did not cause airway inflammation.Conclusion Ozone exposure does not increase allergic sensitization but enhances antigen‐induced airway inflammation in mice that are sensitized via the airways.
Boletus edulis: a digestion‐resistant allergen may be relevant for food allergy
Authors: Helbling A. , Bonadies N. , Brander K. A. , Pichler W. J. 
Published: March 2003

SummaryBackground  Fungal components can cause allergic symptoms either through inhalation, ingestion or contact. Whereas respiratory allergy is thought to be induced by spores, allergic reactions following ingestion are attributed to other parts of the mushroom. Reports of food‐related allergic reactions due to the edible mushroom Boletus edulis have occasionally been reported.Objective  The aim of the study was to investigate whether separate allergens may be detected in alimentary allergy to Boletus edulis.Methods  Sera of two subjects, one with recurrent anaphylaxis and the other with a predominantly oral allergy syndrome following ingestion of Boletus edulis, have been analysed by a time‐course digestion assay using simulated gastric fluid and by SDS‐PAGE immunoblotting. Sera of four Boletus edulis skin prick test‐negative subjects and all without clinical symptoms to ingested Boletus edulis served as controls.Results  In lyophilized Boletus edulis extract, at least four water‐soluble proteins were detected, the most reactive at 55 kDa and at 80 kDa. Following the time‐course digestion assay, IgE binding was found to a 75‐kDa protein, but only if the sera of the subject with recurrent anaphylaxis was used.Conclusion  The data indicate that Boletus edulis can cause an IgE‐mediated food allergy due to a digestion‐stabile protein at 75 kDa. No IgE immune response to this protein was detected in the serum of a subject with respiratory allergy and oral allergy syndrome to Boletus edulis nor in control sera.
An oral introduction of intestinal bacteria prevents the development of a long‐term Th2‐skewed immunological memory induced by neonatal antibiotic treatment in mice
Authors: Sudo N. , Yu X.‐N. , Aiba Y. , Oyama N. , Sonoda J. , Koga Y. , Kubo C. 
Published: March 2003

SummaryBackground Recent epidemiological studies indicate that antibiotic use in infancy may be associated with an increased risk of developing atopy. Our previous work on animals demonstrated that kanamycin use during infancy promotes a shift in the Th1/Th2 balance towards a Th2‐dominant immunity.Objective The first purpose of this study is to clarify whether or not the supplementation of intestinal bacteria can reverse such a Th2‐skewed response induced by neonatal antibiotic use. The second objective is to elucidate the contribution of genetic factors to antibiotic‐induced immune‐deviation.Methods BALB/c or C57BL/6 mice at 3 weeks of age were orally administered 600 µg/day of kanamycin sulphate for seven consecutive days. Thereafter, the mice were inoculated with one type of intestinal bacterial species: Enterococcus faecalis, Lactobacillus acidophilus or Bacteroides vulgatus. Blood samples were collected 10 weeks after the cessation of kanamycin treatment, and the effect of the kanamycin treatment on Th1/Th2 balance was evaluated based on in vivo antibody levels.Results A kanamycin‐induced elevation of the serum IgE levels was reversed by the supplementation with Enterococcus faecalis, and to a lesser extent by that with Lactobacillus acidophilus. The IgE/IgG2a ratio in the mice supplemented with Enterococcus faecalis significantly decreased in comparison with that in the kanamycin‐treated mice without any bacterial supplementation, while such a ratio was enhanced in the mice inoculated with Bacteroides vulgatus. No antibiotic‐induced Th2‐skewed response was seen in C57BL/6 mice that are genetically biased towards Th1‐dominant immunity.Conclusion These results suggest that adequate probiotic intervention after antibiotic treatment may improve the intestinal ecosystem, and thereby prevent the Th2‐shifted immunity induced by neonatal antibiotic use. In addition, the difference of genetic backgrounds also contributes to such an antibiotic‐induced Th2‐skewed response.
β‐Lactam allergenic determinants: fine structural recognition of a cross‐reacting determinant on benzylpenicillin and cephalothin
Authors: Zhao Z. , Baldo B. A. , Rimmer J. 
Published: March 2003

SummaryBackground An appreciation of the structural heterogeneity of allergenic determinants on penicillins and cephalosporins reveals the importance of side‐chain groups and their involvement in many allergies to β‐lactam drugs. Although allergenic cross‐reactions between penicillins and cephalosporins are known to occur, the precise molecular bases of such recognitions and cross‐sensitivities have rarely been studied and identified.Objectives The unexpected finding of a high incidence of positive IgE antibody reactions with both benzylpenicillin and cephalothin prompted serological and immunochemical studies to identify the chemical basis of antibody recognition of these drugs from the two different families of β‐lactam antibiotics.Methods Adsorption studies were employed to identify whether or not a single population of antibodies was involved in the recognition of benzylpenicillin and cephalothin. Identification of the fine structural features recognized by IgE antibodies was investigated by quantitative hapten inhibition studies employing carefully selected β‐lactam drugs, analogues and some other structurally related chemicals.Results Adsorption studies with penicilloic acid‐solid phase clearly established that a single population of cross‐reacting antibodies recognized both benzylpenicillin and cephalothin. Quantitative inhibition findings, especially with phenylacetic acid and 2‐thiopheneacetic acid and with cephaloridine and cefoxitin, which have the same (2‐thienyl)methyl side‐chain as cephalothin, implicated the methylene group as the focus of the allergenic determinant recognized on benzylpenicillin and cephalothin. In addition to the methylene group, recognition graded into neighbouring structures including the amide group and extended weakly to the β‐lactam ring.Conclusions Results confirmed that structural features as small as a methylene group may be allergenically important. In the present case, this group, making up only part of the different side‐chains on benzylpenicillin and cephalothin, together with neighbouring structures extending toward the β‐lactam ring, accounted for the cross‐reactivity seen between structures that, at first sight, appear to be not closely related. Such subtle, small, common structural features are likely to be immunologically recognized and implicated in allergic reactions to other drugs, including β‐lactam antibiotics.
Impact of Mycobacterium vaccae immunization on lung histopathology in a murine model of chronic asthma
Authors: Ozdemir C. , Akkoc T. , Bahceciler N. N. , Kucukercan D. , Barlan I. B. , Basaran M. M. 
Published: March 2003

SummaryBackground Therapeutic modalities of asthma have not been proved to be successful in reversing the already established chronic changes of airways.Objective We aimed to determine the impact of heat‐killed Mycobacterium vaccae immunization, a potent Th1 stimulant, on chronic changes of asthma.Methods Newborn BALB/c mice were divided into three groups; mice in M. vaccae group received 107 colony‐forming units (CFU)/50 µL of heat‐killed M. vaccae subcutaneously on days 3, 14 and 42 before the development of chronic asthma model, whereas mice in control and chronic asthma groups received saline. Subsequently, mice in M. vaccae and chronic asthma groups were administered 10 µg/100 µL of ovalbumin (OVA) on days 43, 45, 47, 49, 51, 53 and 55 intraperitoneally, and 20 µg/10 µL of OVA on days 83, 86 and 89 intratracheally. Mice in control group received saline on the same days.Results Comparison of M. vaccae and chronic asthma groups showed statistically significant differences in goblet cell numbers, thickness of basement membrane and subepithelial smooth muscle of small, medium and large airways and epithelial thickness of medium airways. There was no significant difference between the control and M. vaccae groups except for goblet cell numbers of medium and large airways, and epithelial thickness of medium airways.Conclusion Results of our study suggested that immunization by M. vaccae of newborn mice would prevent some of the chronic changes of airways due to asthma.
Phosphatidylinositol-specific-phospholipase C cleaves urokinase plasminogen activator receptor from the cell surface and leads to inhibition of pemphigus-IgG-induced acantholysis in DJM-1 cells, a squamous cell carcinoma line
Authors: Asano S. , Seishima M. , Kitajima Y. 
Published: March 2003

Abstract
We showed previously that pemphigus IgG enhanced both the activity of urokinase plasminogen activator (uPA) in cultured cells and the expression of its receptor (uPAR) on uPA-binding keratinocytes. In the present study, to clarify whether uPAR and uPA-activated plasmin are actually involved in the blistering process after pemphigus IgG binding to the cell surface, we examined the effects of the following on uPAR expression and on cell–cell detachment in DJM-1 cells, a squamous cell carcinoma line: (i) phosphatidylinositol-specific phospholipase C (PI-PLC) − which releases uPAR from the membrane surface into the culture medium by cleaving the glycosylphosphatidylinositol anchor thus inhibiting uPAR activity, and (ii) uPA inhibitors (tranexamic acid, aprotinin, p-aminobenzonic acid and dexamethasone). Preincubation with PI-PLC decreased dramatically the pemphigus IgG-induced uPAR expression in a dose-dependent manner, and inhibited pemphigus IgG-induced cell–cell detachment at 10 µg/mL. On the other hand, tranexamic acid (15 mm) inhibited pemphigus IgG-induced cell–cell detachment without reduction of uPAR expression, although aprotinin, p-aminobenzonic acid and dexamethasone failed to alter either of these parameters. Although uPAR expression on the pemphigus IgG-bound cell surface and uPA activation may contribute significantly to the pathogenesis of acantholysis in pemphigus, the mechanisms are complicated and should be defined further.
Potential role of B7-1 and CD28 molecules in immunosuppression in leprosy
Authors: Agrewala J N , Kumar B , Vohra H 
Published: March 2003

AbstractIn order to understand the mechanism of unresponsiveness towards Mycobacterium leprae antigens in leprosy, we evaluated the role of M. leprae sonicate antigens in regulating the expression of the costimulatory molecules B7-1, CD28, intercellular adhesion molecule-1 (ICAM-1), LFA-1α, LFA-1β and Mac-1 on the lymphocytes of both leprosy patients and healthy subjects. It was observed that the expression of B7-1 and CD28 was significantly decreased but the levels of ICAM-1 and LFA-1α were increased in patients with untreated borderline leprosy (BL)/lepromatous leprosy (LL) disease. No remarkable change was noticed in the case of borderline tuberculoid (BT) leprosy or treated BL/LL patients. Further, a striking finding was that lymphocytes from healthy subjects cultured with a particularly high dose of M. leprae sonicate antigens down-regulated the expression of B7-1 and CD28 molecules, but up-regulated the display of ICAM-1 and LFA-1α. Furthermore, proliferation induced by M. leprae sonicate was inhibited only by anti-B7-1 antibody. Mycobacterium leprae antigen-induced suppression of the proliferation of lymphocytes of healthy volunteers and LL patients was reversed by culturing the lymphocytes with purified protein derivative (PPD). It may be concluded from the findings in this study that down regulation of B7-1 and CD28 in BL/LL leprosy patients may be responsible for a defective T cell signalling by the B7-1/CD28 pathway caused by M. leprae antigens. This may lead to clonal inactivation of M. leprae-reactive T cells, consequently the bacilli grow without restriction in macrophages.
Serum antibodies to HIV-1 are produced post-measles virus infection: evidence for cross-reactivity with HLA
Authors: Baskar P V , Collins G D , Dorsey-Cooper B A , Pyle R S , Nagel J E , Dwyer D , Dunston G , Johnson C E , Kendig N , Israel E , Nalin D R , Adler W H 
Published: March 2003

SUMMARYConvalescent sera obtained from patients who were recently recovered from an acute measles virus infection were tested for the presence of anti-HIV-1 antibodies by Western blot analysis. While 16% (17/104) of control sera displayed reactive bands to a variety of HIV proteins, 62% (45/73) of convalescent sera demonstrated immunoreactive bands corresponding to HIV-1 Pol and Gag, but not Env antigens. This cross-reactivity appears to be the result of an active measles infection. No HIV-1 immunoblot reactivity (0/10) was observed in sera obtained from young adults several weeks after a combined measles, mumps, and rubella (MMR) vaccination. Interestingly, examination of anti-HLA typing sera specific for either class I and class II molecules revealed that 46% (19/41) of these sera contained cross-reactive antibodies to HIV-1 proteins. Absorption of measles sera with mixed lymphocyte reaction (MLR)-activated lymphocytes and/or HIV-1 recombinant proteins significantly decreased or removed the presence of these HIV-1-immunoreactive antibodies. Together, these findings suggest that the immune response to a natural measles virus infection results in the production of antibodies to HIV-1 and possibly autoantigens.
Increase of CD57+ T cells in knee joints and adjacent bone marrow of rheumatoid arthritis (RA) patients: implication for an anti-inflammatory role
Authors: Arai K , Yamamura S , Seki S , Hanyu T , Takahashi H E , Abo T 
Published: March 2003

SUMMARYThe distribution of CD57+ T and CD56+ T cells in patients with RA was examined. In control osteoarthritis patients, these cells exist as a minor population in the peripheral blood. Our data show that in patients with RA, CD57+ T cell levels are elevated in peripheral blood, knee joint fluid, knee synovial membrane and bone marrow (BM), compared with peripheral blood of controls. CD57+ T cells are especially high in knee joint fluid and joint-adjacent BM, while CD56+ T cells show no such increase. CD57+ T cells contain a major population of CD8+ cells and higher proportions of CD4−8− cells and γδ T cells than do CD57−T cells. CD57+T cells in peripheral blood and joint fluid increase with the duration of disease. Erythrocyte sedimentation rate (ESR) is inversely correlated with the proportion of CD57+T cells in the joint fluid. Although RA frequently occurrs in patients with CD3+57+ cell leukaemia, and some CD57+T cells are likely to be involved in the onset of RA, we suggest that CD57+T cells may rather suppress inflammation of RA, and other cellular components (e. g. granulocytes) may govern the severity of the inflammation of RA. These CD57+ T cells are probably generated extrathymically in the adjacent BM or joint space.
The effect of cyclosporin A, FK506 and rapamycin on the murine contact sensitivity reaction
Authors: Salerno A , Bonanno C T , Caccamo N , Cigna D , Dominici R , Ferro C , Sireci G , Dieli F 
Published: March 2003

SUMMARYWe have evaluated the effects of three potent immunosuppressive agents, cyclosporin A (CsA), FK506 and rapamycin, on the murine contact sensitivity (CS) reaction to the hapten trinitrochlorobenzene. Development of CS reaction requires participation of three distinct T cell subsets: αβ+, CD4+ T lymphocytes, which are the classical effector cell of the CS reaction, γδ+ T lymphocytes, and αβ+, double-negative (CD4− CD8−) T lymphocytes that express the B220 molecule and produce IL-4. We found that all three drugs inhibit the development of the CS reaction, but they affect different target cells. In fact, rapamycin and FK-506 block both αβ+, CD4+ and γδ+ T lymphocytes, while CsA inhibits only the αβ+, CD4+ T lymphocyte. None of the three drugs exerted any inhibitory activity on the αβ+, double-negative (CD4− CD8−) T lymphocytes. Hapten-immune lymph node cells from mice treated in vivo with CsA or FK506 failed to proliferate and to produce IL-2 when re-exposed to the specific antigen in vitro. In contrast, immune lymph node cells from mice that had been treated in vivo with rapamycin gave optimal antigen-specific proliferation and IL-2 production in vitro. The implications of these observations are discussed in relation to the use of these immunosuppressive agents for prevention of allograft rejection.