bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of neutrophil chemotaxis and chemokinesis associated with a plasma protein in aging rats: selective depression of cell responses mediated by complement-derived chemoattractants
Authors: Mello S B V , Farsky S H P , Sannomiya P , Garcia-Leme J 
Published: January 2018

Abstract
The influence of aging on neutrophil chemotaxis, chemokinesis, and superoxide production was investigated in rats. Animals of two age groups, 3 to 4 months and 20 to 21 months, were used. Equivalent neutrophil chemotactic responses to N-formyl-methionyl-leucyl-phenylalanine (fMLP), leukotriene B4 (LTB4), and bacterial lipopolysaccharide (LPS)-activated plasma were observed in both groups of animals, with cells suspended in Hanks' balanced salt solution (HBSS). However, cross-incubation studies in which cells from young adult rats were exposed to plasma from aged donors, then resuspended in HBSS for testing, showed marked changes in the ability of the cells to respond to the chemoattractants. The response to LPS-activated plasma was reduced, whereas responses to fMLP and LTB4 remained unaltered. Previous incubation of the cells with homologous plasma from young donors produced no effect. The inhibitory activity developing with advancing age affected not only chemotaxis but also random movement stimulated by LPS-activated plasma. The inhibitory activity of chemotaxis and chemokinesis in plasma of aged animals was heat labile (56°), vanished in the presence of a proteolytic enzyme like trypsin, and was maintained after dialysis with 12,000-Mr retention dialysis tubing. The material did not influence superoxide production by stimulated neutrophils. It is suggested that inhibition of neutrophil locomotion with advancing age is associated with a plasma protein capable of interacting with neutrophil receptors for complement-derived chemoattractants. The inhibitory substance might influence neutrophil responses to infection and inflammation in the elderly.
Macrophage and lymphocyte functions are down-regulated in newborn rabbits
Authors: Tomai Mark A , Fitzgerald Thomas J , Froberg M Kent 
Published: January 2018

Abstract
We have developed an animal model for congenital syphilis. Treponema pallidum is injected intravenously into pregnant rabbits and fetuses are infected in utero. As a prelude to characterizing the immunologic consequences of fetal infection, it was necessary to expand on the baseline information about newborn rabbit immune capabilities. Studies were undertaken to determine splenic macrophage and T lymphocyte functions with emphasis on newer immunologic parameters. Newborns aged 2 weeks were compared to adults. Macrophage capabilities in newborn rabbits differed from those of their adult counterparts. These cells produced similar basal levels of interleukin 1 (IL-1) but failed to respond to the IL-1 stimulants of lipopolysaccharide (LPS) or T. pallidum. Macrophages also exhibited diminished levels of la expression and increased levels of prostaglandin E2 (PGE2) secretion. T lymphocyte functions were altered in newborn spleen preparations. Following concanavalin A (Con A) stimulation, interferon γ production was half that of adults; in direct contrast, IL-2 production was twice that of adults. Con A–induced lymphocyte proliferation was markedly decreased in newborn preparations. This diminished response resulted from down-regulation rather than immaturity. When newborn splenic cells were stimulated with Con A in the presence of indomethacin, anti-transforming growth factor (anti-TGF), or exogenous IL-1/IL-2, better proliferation resulted. PGE2, which is well established as a down-regulator of newborn immune functions in human and mouse systems, also appears to play a role in suppressing newborn rabbit functions. TGF is a potent suppressor of a number of adult immunologic reactions. This is the first documentation of the potential role of this factor in down-regulating newborn immune capabilities. These findings provide a framework for future investigations of our congenital syphilis model.
Carcinoembryonic antigen binding proteins on elicited peritoneal macrophages
Authors: Ann Toth Carol 
Published: January 2018

Abstract
Carcinoembryonic antigen (CEA), a member of the immunoglobulin supergene family, is recognized by a specific 80-kd receptor on Kupffer cells and alveolar macrophages. Peritoneal macrophages were harvested from male Sprague-Dawley rats 72 h after intraperitoneal injection with thioglycolate broth and from unstimulated animals. The elicited peritoneal macrophages had a much greater capacity to endocytosed CEA than the cells isolated from unstimulated animals. They took up CEA in a concentration- and time-dependent manner. Cellular uptake was temperature and colchicine sensitive indicating internalization of CEA. The process was saturable and could be specifically inhibited by CEA and nonspecific crossreacting antigen (NCA), a member of the CEA supergene family. Two binding proteins of ~ 35 and 80 kd were isolated from the surface of the peritoneal macrophages by affinity chromatography on a CEA-Sepharose column. Using CEA coupled to sulfo-succininidyl-2-[p-azidosalicyl amide]-1,3′-dithiopropionate (SASD), a photoactivatable crosslinker, two binding proteins of 55 and 80 kd were identified on the surface of live peritoneal macrophages. The specificity of CEA endocytosis and binding proteins exhibited by the elicited peritoneal cells are similar to that previously reported for Kupffer cells and alveolar macrophages.
Monoclonal antibody NIMP-R10 directed against the CD11b chain of the type 3 complement receptor can substitute for monoclonal antibody 5C6 to exacerbate listeriosis by preventing the focusing of myelomonocytic cells at infectious foci in the liver
Authors: Conlan J Wayne , North Robert J 
Published: January 2018

Abstract
Treatment of mice with a monoclonal antibody (mAb) designated NIMP-R10, directed against the CD11b polypeptide of the CD18/CD11b heterodimeric type 3 complement receptor (CR3), exacerbates listeriosis by preventing myelomonocytic cells from focusing at sites of infected hepatocytes in the liver. Under these conditions an otherwise sublethal Listeria inoculum grows unrestrictedly within hepatocytes and causes death in 3 days. The results obtained with NIMP-R10 are similar to those previously obtained with a different anti-CD11b mAb (5C6), although mAb NIMP-R10 is more effective at enhancing infection. Therefore, both mAbs can be used to analyze host antibacterial defenses in vivo.
Postreceptor events associated with human neutrophil activation by interleukin-8
Authors: Smith Robert J , Sam Laurel M , Leach Karen L , Justen James M 
Published: January 2018

Abstract
Recombinant human monocyte–derived interleukin-8 (IL-8M), recombinant human endotheliumderived IL-8 (IL-8E), and a recombinant human truncated form of IL-8 (IL-8T) stimulated a time-dependent (t1/2 ~ 2–3 s) and concentration-dependent (0.1–100 nM) release of azurophil (myeloperoxidase) and specific (vitamin B12 binding protein, gelatinase) granule constituents from cytochalasin B–treated human neutrophils (HNs) wherein IL-8T = IL-8M &gt; IL-8E. An increase in the cytosolic free calcium concentration ([Ca2+]i) was greater in IL-8T– than in IL-8M– or IL-8E–activated HNs, and IL-8T was more potent than either IL-8M or IL-8E in sequentially desensitizing the HNs to the effects of the other IL-8 forms. IL-8 induced a time- and concentration-dependent (0.1–100 nM) increase in the production of inositol 1,4,5-trisphosphate (IP3) in HNs. U-73122 (1-[6-[[17β-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione), a potent inhibitor of phospholipase C–catalyzed events in HNs, suppressed IL-8–triggered IP3 production, increased [Ca2+]i and granule exocytosis in HNs. The membrane-associated activity of the α and β subtypes of protein kinase C was significantly enhanced in IL-8–activated cells.
Wheat germ agglutinin inhibits the C5a receptor interaction: implications for receptor microheterogeneity and ligand binding site
Authors: Johnson Richard J , Simpson Stacy , van Epps Dennis E , Chenoweth Dennis E 
Published: January 2018

Abstract
Wheat germ agglutinin (WGA) has been shown to inhibit the interaction of C5a with the C5a receptor on both polymorphonuclear neutrophils (PMNs) and the histiocytic cell line U937. The level of inhibition with isolated receptor preparations is 100%, and on intact cells 10 to 20% of the receptor population appear to retain their ability to bind C5a in the presence of WGA. In contrast, this lectin completely inhibits the C5a-mediated degranulation of PMN primary and secondary granules, suggesting that the population of C5a receptors responsible for mediating degranulation is also recognized by WGA. More than 50% of the receptors appear to be blocked before an effect on degranulation occurs. This inhibition by WGA does not appear to be due to down-regulation of C5a receptors from the cell surface, excessive aggregation of receptor sites, or interaction of WGA with the carbohydrate portion of the C5a molecule. The inhibition is reversed by N-acetylglucosamine but not by sialic acid. This effect appears to be specific for WGA because various other lectins do not inhibit the C5a receptor interaction. That the inhibition by WGA is due to direct binding of the lectin to N-acetylglucosamine residues on the C5a receptor is strongly supported by the ability of the cross-linked C5a-receptor complex to bind to and be specifically eluted from a WGA-Affigel affinity matrix. These observations are consistent with hypothesis that the population of C5a receptors on leukocytes exhibits microheterogeneity with respect to structure (carbohydrate content) and/or function. J. Leukoc. Biol. 52: 3–10; 1992.
Direct interaction between an antigen-specific B cell clone and an MHC class II–reactive helper T cell clone
Authors: Hamano Teruaki , Asano Yoshihiro , Iwasaki Tsuyoshi , Yamasaki Tadakuni , Hase Kazunobu , Kakishita Eizo 
Published: January 2018

Abstract
TP67.14 established by somatic hybridization is a 2,4,6-trinitrobenzenesulfonic acid (trinitrophenyl, TNP)-specific B cell clone with a receptor molecule for TNP on the cell membrane, and MS202 is an interleukin-2 (IL-2)–dependent T helper (Th) cell clone reactive to auto-MHC class II antigens (IAk and IEk) as previously reported. In the present study it was shown that MS202 considerably induced the maturation of TP67.14 into anti-TNP plaque-forming cells (PFCs), and this response was markedly augmented by the addition of TNP–keyhole limpet hemocyanin (KLH). Recombinant cytokines and the culture supernatant of MS202 with TP67.14 did not affect the generation of anti-TNP antibodies by TP67.14. Also, neither anti–IL-4 nor anti–IL-5 monoclonal antibody (mAb) inhibited the maturation of TP67.14 mediated by MS202. The differentiative effect of MS202 on TP67.14 was completely lost when each cell was separately cultured using a semipermeable membrane. Monoclonal antibodies against LFA-1β molecules significantly blocked the development of anti-TNP PFCs induced by MS202, as well as anti-IAk and anti-IEk ImAbs. Interestingly, the plasma membrane–enriched fraction (PM) derived from MS202 exhibited much more differentiative effects on TP67.14 treated with TNP-KLH than PM from other T cell lines and concanavalin A–induced T lymphoblasts. In addition, TNP-conjugated PM from MS202 by itself induced a great number of anti–TNP PFCs. The present findings indicate that MS202 is capable of inducing the maturation of TP67.14, which is considered to represent a population of B cells with antigen specificity in a late lineage of B cell maturation, through direct cell contact but not soluble factors. This suggests that B cells with antigen specificity, in the presence of antigen, can be induced to mature into antibody-secreting cells through direct contact with Th cells; in this process surface major histocompatibility complex class II and lymphocyte function-associated antigen 1 (LFA-1) molecules are directly involved and the cell membrane derived from Th cells provides a transductional signal for maturation of B cells with antigen specificity in the presence of antigen.
Differences in the onset of the inflammatory response to cutaneous leishmaniasis in resistant and susceptible mice
Authors: Beil Waltraud J , Meinardus-Hager Georg , Neugebauer Dorothea-Ch , Sorg Clemens 
Published: January 2018

Abstract
Sites of cutaneous infection with Leishmania major in genetically susceptible (BALB/c) and resistant (C57B1/6) mice were investigated for the early inflammatory response (6 h to 12 days) by electron microscopy combined with enzyme-histochemical methods. Susceptible BALB/c mice spontaneously recruited only polymorphonuclear leukocytes (PMNs) at the site of infection. Infiltrating mononuclear phagocytes (and eosinophils) were first observed at day 1 in a ratio equal to the influx of PMNs (about 40%). This pattern persisted during the following 11 days of infection. In the resistant C57/B16 mice, the first cellular infiltrate at the infected site contained mononuclear phagocytes (25%) and eosinophils (15%) besides PMNs (60%). Within 3 days after infection, mononuclear phagocytes became the dominant population of cells in cutaneous lesions (up to 80%). It was found in situ that L. major accumulated and replicated in immature macrophages, that is, intermediate stages between monocytes and resident macrophages, which were found in lesions of both strains. The burden of parasites was, however, degraded more rapidly by the infiltrating cells of the resistant mice than by those of the susceptible ones. Within the first 4 days of infection, the parasites were found in PMNs, mononuclear phagocytes, and extracellular spaces in both strains. In susceptible mice this distribution pattern persisted up to 12 days after infection; in resistant C57B1/6 mice parasites accumulated inside mononuclear phagocytes within this period. It is concluded that the features of acute inflammation during leishmaniasis in BALB/c mice are sustained over a prolonged period that is ineffective in the elimination of L. major.
Macrophage antimicrobial functions in a chicken MHC chromosome dosage model
Authors: Lin H-K , Bloom SE , Dietert RR 
Published: January 2018

Abstract
Macrophages respond to certain inflammatory signals with a marked increase in respiratory burst and the production of reactive oxygen intermediates; these metabolites play an essential role in the destruction of invading microorganisms. In this study, macrophage antibacterial inflammatory responses were compared among chickens having two (disomic), three (trisomic), or four (tetrasomic) copies of the major histocompatibility complex (MHC)–encoding microchromosome (B15 haplotype). Phorbol myristate acetate (PMA)–stimulated superoxide anion (O2-) production by cross-linked dextran (Sephadex)–elicited peritoneal macrophages was measured at early (4 h), intermediate (24 h), and late (42 h) stages of the inflammatory response using ferrocytochrome c reduction. Significantly elevated O2- production was observed for trisomic versus disomic macrophages during both early and intermediate stages of the inflammatory response. Late in the response, tetrasomic macrophages produced a significantly higher level of O2- than disomic cells. When PMA was used to trigger hydrogen peroxide (H2O2) production, no significant genotype difference was found for any stage of the inflammatory response. Phagocytosis of heat-killed Salmonella enteritidis by macrophages differed among the three genotypes: trisomic macrophages were superior to disomic cells during early inflammation, no genotypic difference was observed at the intermediate stage, and disomic cells had greater phagocytic capacity than aneuploid macrophages late in the response. Likewise, when S. enteritidis was cultured with macrophages to induce oxygen intermediate secretion, H2O2 production followed a kinetic pattern among the genotypes similar to that observed for bacterial phagocytosis. Endogenous superoxide dismutase (SOD), catalase, and glutathione peroxidase (GP) activities were determined for the macrophages during intermediate and late inflammatory stages. Tetrasomic macrophages had reduced SOD activity at the late stage, no significant difference was observed in catalase activity among genotypes at either time point, and trisomic macrophages had enhanced GP activity compared to disomic cells at both time points. These results indicate that differences in MHC gene dosage are associated with differences in chicken macrophage activation for the acquisition of selected antibacterial functions.
Substrate-specific proteases (BLT-esterase) are localized predominantly in the natural killer cells of unprimed mice
Authors: Savers Thomas J , Mason Llewellyn H , Pilaro Anne , Wiltrout Theresa A , Komschlies Kristin , Munger William L , Wiltrou Robert H 
Published: January 2018

Abstract
In leukocytes isolated from unprimed mice, the levels of extractable Nα-Cbz-Lys-thiobenzylester- esterase (BLT-esterase) closely correlated with the number of natural killer (NK) cells. The spleens of mice that exhibit severe combined immunodeficiency (SCID) contained much higher levels of this enzyme than other mouse strains. Treatments that resulted in a local accumulation of NK cells (as assessed by lytic activity) produced a concomitant increase in BLT-esterase activity. However, short-term in vitro treatment of spleen cells with interferon (IFN)-α/β indicated that BLT-esterase levels correlated more closely with absolute numbers of NK cells than with their lytic capacity. There was a very good correlation between the numbers of cells bearing the NK phenotype (NK-1. 1+) and BLT-esterase levels. Cells positively sorted using the NK-specific antibodies NK-1. 1 and LGL-1 had high enzymatic activity. The BLT- esterase levels were high in both the NK-1. 1+LGL-1” and NK-l. r/LGL-r subsets. Highly purified CD4+ and CD8+ T cells and slg+ B cells demonstrated negligible enzyme, as did populations of cells highly enriched for macrophages or neutrophils. However, it should be stressed that the inbred mice used on this study have been maintained in a pathogen-free facility. It would be anticipated that mice maintained under less stringent conditions could exhibit appreciable levels of BLT-esterase activity in their T cells. Nonetheless, BLT-esterase is present at high levels in NK cells and cannot be regarded as a T cell-specific enzyme. J. Leukoc. Biol. 53: 454–461; 1993.
Endocytosis of ß2 integrins by stimulated human neutrophils analyzed by flow cytometry
Authors: Chambers J David , Simon Scott I , Berger Elaine M , Sklar Larry A , Arfors Karl-E 
Published: January 2018

Abstract
Flow cytometry and fluorescently labeled monoclonal antibodies were used to investigate endocytosis of human neutrophil ß2 integrins following cellular activation. GDI 8 initially present on the cell surface cycled in two phases after exposure to formyl peptide or plateletactivating factor. The first phase lasted 3 min at 37°C; after a lag, CD18 was specifically internalized at approximately 20%/min. Subsequently a second phase was detectable consisting of exponential reduction of internal fluorescence with a half-time of approximately 2 min, representing probe reexpression. At peak endocytosis approximately 40% of CD18 was internalized. All of the internalized CD18 was associated with αM (CR3); no endocytosis of αL (LFA-1) was observed. When neutrophils were stimulated with phorbol esters or calcium iono- phore, CD18 was internalized much more slowly (t1/2 = 5 min) and probe was not reexpressed. Endocytosis of CD18 may participate in regulating neutrophil adhesiveness, removing activated receptors, or permitting receptor recycling. J. Leukoc. Biol. 53: 462–469; 1993.
In vivo immortalization of murine peritoneal macrophages: a new rapid and efficient method for obtaining macrophage cell lines
Authors: Adami Cecilia , Brunda Michael J , Palleroni Alicia V 
Published: January 2018

Abstract
Although several murine macrophage (mφ) cell lines from different sites have previously been obtained by in vitro infection with the J2 murine retrovirus, which carries the v-raf and v-myc oncogenes, it was not possible to immortalize thioglycolate-elicited peritoneal macrophages (Pmφs) by this in vitro procedure. A technique utilizing in vivo injection of the J2 virus has been developed to overcome this problem. The J2 virus immortalized Pm φs in a very efficient manner in vivo because no exogenous growth factors were required for the in vitro proliferation of these cells and numerous continuous cloned cell lines were readily established. In contrast, Pmφs obtained from uninfected mice or Pmφs infected in vitro with the J2 virus did not proliferate. The in vivo immortalized cells had many of the morphological and functional characteristics of mφs. Analysis of two of the clones, PMJ2-PC and PMJ2-R, demonstrated intracellular expression of the product of the v-raf gene, presence of mφ-associated cell surface antigens, interleukin-6 secretion induced by lipopolysaccharide, and biological response modifier-induced cytotoxic activity against tumor cells. In addition, one of the clones, PMJ2-PC, constitutively expressed major histocompatibility complex (MHC) class II antigens, and in the other clone, PMJ2-R, MHC class II antigen expression was induced by recombinant murine interferon-γ. This method of utilizing the J2 virus in vivo represents a novel technique for obtaining hematopoietic cell lines from cells that are difficult to immortalize in vitro. J. Leukoc. Biol. 53: 475–478; 1993.
Monoclonal antibodies to the carbohydrate structure Lewisx stimulate the adhesive activity of leukocyte integrin CD11b/CD18 (CR3, Mac-1, αmβ2) on human granulocytes
Authors: Stöckl Johannes , Magdic Otto , Rosenkranz Alexander , Fiebiger Edda , Kniep J Bernhard , Stockinged Hannes , Knapp Walter 
Published: January 2018

Abstract
Several carbohydrate structures on human granulocytes have been discussed as potential ligands for C- type lectins (selectins) on endothelial cells. Among them are the lacto-series type II chain antigens sialyl-Lewisx (SLex), Lewisx (Lex), and VIM2. We demonstrated in this study that monoclonal antibodies (mAbs) to Lex and to SLex, but not other anticarbohydrate mAbs (VIM2, CDwl7, CD24), can stimulate granulocytes to form homotypic aggregates. This effect was particularly noticeable with three distinct anti-Lex mAbs (3C6, 4D1, 6C7). Much less impressive effects were also seen with nine other anti-Lex mAbs and with the anti-SLex mAb CSLEX1. Aggregation was shown to be an active process. It is temperature and energy dependent, requires divalent cations, and is selective in terms of mAb specificity. Anti- Lex-induced homoaggregate formation could be inhibited with CDllb mAb JML-H11 and CD54 (ICAM1) mAb LB-2 and thus seems to be associated with activation of the β2-integrin cytoadhesion pathway. J. Leukoc. Biol. 53: 541–549; 1993.