Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of the receptor CD11b/CD18 on the polymorphonuclear leukocyte (PMN) surface is important for several aspects of PMN function during endotoxemia. The mechanisms underlying regulation of CD11b/CD18 expression during hypoxemia and endotoxemia, however, are less clear. We investigated the effects of exposure of whole blood PMNs to lipopolysaccharide (LPS) during hypoxemia. During hypoxemia (10-30% O2 saturation), LPS reduced CD11b/CD18 expression. Both kinetic assays and experiments with microfilament stabilizers (phalloidin, cytochalasin B) demonstrated that this was most likely due to receptor shedding. Incubation of whole blood PMNs with an anti-CD14 monoclonal antibody (MEM18) largely prevented the LPS-induced reduction of CD11b/CD18 expression. Decreased CD11b/CD18 expression reduced PMN functional capability, as the binding of its ligand (erythrocytes opsonized with the 3rd component of complement Cbi) and intracellular H2O2 production were reduced. After exposure to LPS, N-formyl-methionyl-leucyl-phenylalanine could rapidly induce new CD11b/CD18 receptors to the cell surface, and this was not inhibited by actinomycin D or cycloheximide. After reoxygenation (> 90% O2 saturation), CD11b/CD18 expression was restored, and this was abrogated by exposure to cytochalasin B. Lipid A was able to reproduce the effects of LPS during hypoxemia and hypoxemia-reoxygenation but required a 10-fold greater concentration to do so. These results demonstrate that during hypoxemia an important pathophysiological property of LPS is to reduce CD11b/CD18 expression. This results in diminished PMN functional capability, which would contribute to the pathogenicity of LPS during acute infectious states.
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PMID:Hypoxemia regulates effect of lipopolysaccharide on polymorphonuclear leukocyte CD11b/CD18 expression. 791 25

Cells of monocytic lineage (Mo) persistently infected with human immunodeficiency virus (HIV) have been suspected to be a major reservoir for in vivo transmission of virus to susceptible target cells. Cellular events and mechanisms that upregulate viral gene expression in such cells are important issues. Because the traffic of such cells is central to biodistribution of HIV, we have explored the impact of interaction of endothelium with HIV-1-infected U1 promonocytic cells. Coculturing of U1 with human umbilical endothelial cells (HUVEC) for 24 to 72 hours in the absence of stimulation induced HIV-1 p24 biosynthesis significantly. Antibody-blocking experiments indicated that CD11/CD18 integrins play a role in upregulation of HIV expression elicited by interaction with HUVEC. Engagement of CD11b/CD18 by adherence of U1 to surfaces coated with either the cognate ligand fibrinogen or monoclonal antibody specific for CD11b/CD18 also enhanced p24 biosynthesis. Furthermore, endothelial cells were found to constitutively synthesize and secrete soluble factors that enhanced HIV-1 synthesis. The enhancing factors, of estimated size 10 to 45 kD, were induced in HUVEC to high levels by monokines or by lipopolysaccharide, resulting in markedly enhanced HIV-1 expression by U1. These endothelial cell-derived HIV-1-enhancing factors consist of, among others, interleukin-6 (IL-6), IL-1 beta, and granulocyte-macrophage CSF (GM-CSF). Our results suggest that activation of HIV biosynthesis in infected Mo via interaction with endothelium may impact significantly on the tissue distribution and pathogenesis of HIV infections.
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PMID:Upregulation of human immunodeficiency virus-1 in chronically infected monocytic cell line by both contact with endothelial cells and cytokines. 791 48

A culture system for bovine bone marrow derived macrophages (BBMM) was devised, starting with bone marrow cells from tibiae of calf fetuses of over 6 months gestation. Tibiae removed aseptically were sawed open, and the bone marrow was collected, washed and placed in hydrophobic (teflon) containers, thereby allowing the propagation and differentiation of macrophage lineage cells. All other cell types were negatively selected for. This results in enriched macrophage populations between 12 and 18 days of culture which were suitable for use in functional studies. The culture system was strictly serum-dependent but independent of the addition of conditioned medium containing macrophage colony-stimulating factor. The cells were mature macrophages by morphological and histochemical criteria. They expressed CD14 and CD11b, two typical macrophage markers. They were positive for CD18 and CD36 and bound monomeric murine IgG2a, indicating that a high-affinity Fc receptor for this isotype is expressed by bovine macrophages. The cells ingested erythrocytes opsonized by rabbit IgG, human IgG, bovine IgG1 and IgG2. Upon triggering with opsonized zymosan or phorbol 12-myristate 13-acetate, reactive oxygen species were generated. Upon triggering with lipopolysaccharide, BBMM expressed enhanced amounts of procoagulant activity and secreted cytokines, such as tumor necrosis factor and transforming-growth-factor-beta. These criteria identify the cultured cells as resting macrophages.
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PMID:Generation and functional characterization of bovine bone marrow-derived macrophages. 794 5

We here report the finding that the anti-inflammatory cytokine interleukin-10 (IL-10) inhibits motility of B lymphocytes. B cells were induced to display motile morphology and active migration by IL-4. IL-10 inhibited locomotor responses to IL-4, when B cells of both murine and human origin were used. The inhibitory effect of IL-10 was reversible, since washing of B cells preincubated in IL-10 restored the ability to respond to IL-4. Time-course experiments showed that IL-10 did not have to be present from the very onset of culture, but could be added as late as 5 hr after initiation. In addition, murine B cells stimulated with lipopolysaccharide (LPS) showed motile morphology, as well as cellular aggregation and proliferation. All these parameters were suppressed by IL-10. However, viability of B cells was not adversely affected by IL-10. Exposure to IL-10 did not result in any changes in the surface expression of molecules involved in adhesion, such as CD2, CD11a/CD18, CD44, CD54 or L-selectin, on B lymphocytes.
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PMID:Interleukin-10 inhibits motility in murine and human B lymphocytes. 795 71

The 70Z/3 cell line is able to undergo lineage conversion from a pre-B to macrophage phenotype. Data presented here show that the transition from pre-B to macrophage follows a reproducible pathway via a stable intermediate stage. The cells in the intermediate stage are adherent and have lost the ability to respond to lipopolysaccharide or interferon-gamma by induction of immunoglobulin kappa light chains. However, these cells do not yet display the full range of macrophage-specific properties such as receptors for macrophage-colony stimulating factor or the beta 2 integrin CD11b/CD18. Subcloning experiments with the intermediate cells revealed that they retain the options of either persisting along the macrophage line of differentiation, acquiring additional macrophage traits, or reverting to the pre-B phenotype. Further differentiation to the macrophage stage is accompanied by the apparent loss of the ability to revert. Thus, these studies define relationships among lineage-specific traits, and begin to reveal critical stages in lineage commitment.
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PMID:Characterization of the B cell-macrophage lineage transition in 70Z/3 cells. 802 17

Nitric oxide (NO) is produced by murine macrophages in response to cytokines and/or gram-negative bacterial lipopolysaccharide. NO induction by gram-positive bacteria such as group B streptococci (GBS), the major etiologic agents of neonatal pneumonia and meningitis, has received little study. GBS as well as two other gram-positive bacterial species, Staphylococcus aureus and Staphylococcus epidermidis, were found to stimulate NO production in thioglycolate-elicited murine macrophages and in the mouse macrophage cell line J774A.1 in the presence of gamma interferon. Serotype Ia and III GBS were both stimulatory, as were asialo- and type antigen-deficient mutant strains of type III GBS. NO production was dose dependent, inhibitable by L-arginine analogs, and unaffected by polymyxin B. Since phagocytosis by murine and human phagocytes of GBS is dependent on complement receptor type 3 (CR3), the role of CR3 in the NO response to GBS was tested in the CR3-deficient myelomonocytic cell line WEHI-3. GBS did not induce NO, whereas S. aureus or lipopolysaccharide did induce NO in WEHI-3 cells. S. epidermidis, whose nonopsonic phagocytosis is also CR3 dependent, failed to induce NO in WEHI-3 cells. Monoclonal anti-CR3 (anti-CD11b or anti-CD18) in the presence of interferon also induced NO production in thioglycolate-elicited macrophages and in J774A.1 cells but not in WEHI-3 cells. This evidence suggests that ligated CR3 and gamma interferon act synergistically to induce NO production and that CR3 mediates the GBS-induced signal for NO production in interferon-treated macrophages.
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PMID:Group B streptococcus-induced nitric oxide production in murine macrophages is CR3 (CD11b/CD18) dependent. 803 77

Secretion of unique eosinophil granule constituents may play a role in allergic and parasitic reactions. Therefore we have investigated possible mechanisms for regulation of secretion in eosinophils. A hemolytic plaque assay and an enzyme-linked immunospot (ELISPOT) assay were developed for detection of secreted eosinophil cationic protein (ECP) from single adherent eosinophils. The protein kinase C activator phorbol 12-myristate 13-acetate (PMA) induced release of ECP in a dose-dependent fashion but 4-alpha-PMA, an analogue that does not activate protein kinase C, did not cause degranulation. Staurosporine and K252a, inhibitors of protein kinase C, decreased PMA-induced ECP secretion. Low concentrations of cytochalasin B enhanced PMA-induced secretion but high concentrations had an inhibitory effect. The calcium ionophores A23187 and ionomycin were weaker secretagogues than PMA. Tumor necrosis factor, granulocyte-macrophage colony-stimulating factor, interleukin-3, interleukin-5, N-formylmethionyl-leucyl-phenylalanine, and lipopolysaccharide caused little or no degranulation in adherent eosinophils. Preincubation of eosinophils with antibodies to CD18, the common beta chain of leukocyte adhesion proteins, resulted in inhibition of PMA-induced ECP release from adherent cells. 1,2-Bis(O-aminophenyl)-ethane-ethane-N,N,N',N'-tetraacetic acid (BAPTA), an agent that acts intracellularly by chelation of calcium, also inhibited PMA-mediated ECP release. In conclusion, PMA induces release of ECP from single adherent eosinophils and the effect appears to be mediated via protein kinase C and, in contrast to that in neutrophils, to be dependent on CD11/CD18 leukocyte integrins.
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PMID:Phorbol ester-induced degranulation in adherent human eosinophil granulocytes is dependent on CD11/CD18 leukocyte integrins. 809 65

Several functions of polymorphonuclear cells (PMNs) require adhesion to occur. Various membrane proteins' functions such as CD18 (beta 2 chain of integrin), CD35 (CR1) and CD16 (F c gamma Receptor III) participate in adhesion. In vivo treatment with Ribomunyl (R), an immunomodulating agent, was shown to enhance adhesion and migration of PMNs. To explore the direct effect of R on PMNs, cells from healthy subjects were treated in vitro with R. A significant increase of PMN adhesion and expression of CD18 and CD35 molecules were observed with 50 and 100 micrograms/ml of R after 2 h incubation. However, R-treatment decreased the PMN reactivity towards anti-CD16 (F c gamma RIII) monoclonal antibody. The effect of R on adhesion and membrane molecule expression was independent of the presence of serum and of polymixin B. Thus, this effect cannot be due to lipopolysaccharide (LPS) contaminants and does not require interactions with serum components. In previous studies, it was shown that in vitro amoxicillin increased some PMN functions whereas josamycin decreased them. The in vitro incubation of PMNs with R and amoxicillin (100 micrograms/ml) potentiated the positive effect of amoxicillin on adhesion and the antibiotic counterbalanced the negative effect of R on CD16 expression. In addition, R compensated the negative effect of josamycin (100 micrograms/ml) on PMN adhesion and on CD18 and CD35 expression. This study indicates: (1) the direct effect of R on PMN adhesion and on expression of molecules involved in adhesive-mediated functions, and (2) the beneficial effect of the association of R with antibiotics which can stimulate PMN activity.
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PMID:In vitro stimulation of polymorphonuclear cell adhesion by ribomunyl and antibiotic + ribomunyl combinations: effects on CD18, CD35 and CD16 expression. 809 33

Cell adhesion molecules are surface proteins important for cell migration and adhesion and are strongly expressed in eyes with inflammation. We studied the expression of two cell adhesion molecules: intercellular adhesion molecule-1 (ICAM-1, CD54) and lymphocyte function-associated antigen-1 (LFA-1, CD11a/CD18) in mice with experimental autoimmune uveitis. B10.A mice were immunized with interphotoreceptor retinoid-binding protein and eyes were serially examined for expression of cell adhesion molecules using immunohistochemical staining. ICAM-1 was expressed on the vascular endothelium of the ciliary body and retina by 7 days after immunization, and LFA-1 was first expressed on some infiltrating inflammatory cells 9 days after immunization. Clear histologic evidence of ocular inflammation did not occur until 11 days after immunization. We then studied the effect of monoclonal antibodies against ICAM-1 and LFA-1 on the development of experimental autoimmune uveitis. Three groups of mice were immunized and treated for 21 days with daily intraperitoneal injections of rat monoclonal antibody against murine ICAM-1 or LFA-1 or with rat IgG as control. Ocular inflammation, graded clinically by examination of the fundus 14 and 21 days after immunization, was significantly decreased in animals treated with anti-ICAM-1 (P < 0.01 at Days 14 and 21) and with anti-LFA-1 antibody (P < 0.01 at Days 14 and 21). The intraocular inflammation graded histologically was also decreased in mice treated with anti-ICAM-1 and anti-LFA-1 antibody. This difference in the histologic grade of inflammation was statistically significant (P < 0.02) between mice treated with anti-ICAM-1 antibody and control mice and approached statistical significance (P < 0.10) in mice treated with anti-LFA-1 antibody compared to the control mice. Proliferative responses to lipopolysaccharide, PPD, and interphotoreceptor binding protein of lymphocytes obtained from the draining lymph nodes of mice treated with the antibodies were lower than those from the control mice, suggesting that cell-cell binding was impaired in treated mice. These data show that ICAM-1 is expressed in the eye before histologic evidence of inflammation, and that monoclonal antibodies against ICAM-1 and LFA-1 are effective in inhibiting experimental autoimmune uveitis in mice.
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PMID:Monoclonal antibodies against ICAM-1 (CD54) and LFA-1 (CD11a/CD18) inhibit experimental autoimmune uveitis. 810 Jan 90

We have examined the role of cell adhesion molecules in the homotypic aggregation of rat alveolar macrophages after exposure to wool and grain dusts. Molecules such as bacterial lipopolysaccharide (LPS) and phorbol myristate acetate (PMA) can upregulate adhesion molecules, resulting in aggregation of lymphocytes. In rats treated intratracheally with an inspirable sample of wool dust collected from the air of British wool textile mills, and sieved grain dust, aggregates of macrophages were present in the bronchoalveolar lavage (BAL). Our hypothesis was that substances present on the dust surface could activate and upregulate adhesion molecules of the CD11/CD18 complex on the BAL cells and account for the aggregates. Macrophages from untreated rats form aggregates in vitro, which averaged 19 cells/aggregate; when treated with both wool and grain dusts, this rose to 25 and 24 cells/aggregate, respectively. LPS, PMA, and the proinflammatory cytokine tumor necrosis factor (TNF) also caused increases in aggregate size. Staurosporine, an inhibitor of protein kinase C (PKC), reduced the number of cells per aggregate from 35 cells/aggregate in LPS- and PMA-treated macrophages to 18 cells/aggregate, the same as untreated. In contrast, staurosporine had no effect in reducing the size of aggregates produced by the organic dusts. Removal of divalent cations, which are essential for maintaining integrin stability and PKC activity, resulted in complete abolition of aggregate formation. Treatment with monoclonal antibodies to lymphocyte function-associated antigen-1 (LFA-1) alpha and beta and intercellular adhesion molecule-1 (ICAM-1) resulted in the inhibition of aggregate formation in a dose-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:LFA-1 and ICAM-1 in homotypic aggregation of rat alveolar macrophages: organic dust-mediated aggregation by a non-protein kinase C-dependent pathway. 810 15


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