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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been reported previously that enriched populations of mouse thymus-dependent (T) lymphocytes could be prepared by the use of a column procedure that is believed to remove selectively cells with receptors for antigen-antibody complexes. In our hands, this procedure does not selectively remove B lymphocytes but rather masks the surface immunoglobulin. Analysis of the column-passed cells revealed an apparent decrease in the percentage of immunoglobulin-bearing cells but little decrease in either the percentage of complement receptor lymphocytes or the mitogenic response to lipopolysaccharide. Furthermore, rabbit immunoglobulin could be detected on the surface of 35 to 45% of the cells emerging from the columns prepared with rabbit anti-human gamma-globulin (HGG). After overnight incubation, 30 to 40% of the emerging cells reexpressed mouse immunoglobulin on their surfaces. Adsorption of the antisera used to make the columns with mouse gamma-globulin (MGG) diminished the depleting capacity of the columns. We conclude from these observations that antibodies in the anti-HGG sera, cross-reactive with mouse immunoglobulin, account for the spacious depletion of B lymphocytes observed when cells are passed over these antigen-antibody complex columns.
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PMID:Lack of B lymphocyte depletion from murine spleen cell populations by a human gamma-globulin, anti-human gamma-globulin column system. 4 52

B cells that carry the complement receptor (CR+) were separated from B cells that lack the complement receptor (CR-) by velocity sedimentation or by passage through C-coated Sephadex columns. The kinetics of responses to bacterial lipopolysaccharide (LPS) in both B cell subpopulations were determined in three assay procedures: 1) incorporation of radioactive thymidine into DNA; 2) incorporation of radioactive leucine into immunoglobulin; 3) enumeration of cells forming polyclonal antibody to the 2,4,6-trinitrophenyl hapten. Although both subpopulations of B cells responded to LPS, they differed in the time course. CR- B cells responded with a delay of approximately 24 hr as compared with the response of CR+ B cells. The implications to the ontogenetic status of CR+ and CR- B subpopulations are discussed.
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PMID:Polyclonal activation of CR+ and CR- B lymphocytes: the kinetics of initiation of DNA and immunoglobulin synthesis by lipopolysaccharide. 30 44

The presence of two subpopulations in mouse B lymphocytes responding to pokeweed Pa-1 mitogen or bacterial lipopolysaccharide (LPS) in terms of DNA synthesis was demonstrated. The analysis of surface markers of these two subpopulations revealed that one of the subpopulations carried the complement receptor (CR+) and the other lacked the complement receptor (CR-). The kinetics of stimulation by Pa-1 and LPS differed between these two subpopulations. CR+ -B cells exhibited the first peak of DNA synthesis 27 h after the addition of the mitogen, whereas CR- -B cells showed the first maximal response after 39 h. When the responses of CR+ -B cells 27 h and of CR- -B cells 39 h after various pulsed exposures to the mitogen were compared with those after continuous exposures to the mitogen, two successive 3 h exposures (0-3 and 12-15 h for CR+ -B cells; 0-3 and 21-24 h for CR- -B cells) yielded the same level of response as continuous exposure for 27 h (CR+ -B cells) or 39 h (CR- -B cells). These results indicate that both B-cell subpopulations require two signals for maximal stimulation.
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PMID:Kinetics of B-lymphocytes stimulation by pokeweed Pa-1 mitogen and bacterial lipopolysaccharide. 31 63

A highly purified preparation of mouse B cells showed greatly decreased incorporation of [6-3H]-thymidine when stimulated with pokeweed Pa-1 mitogen or bacterial lipopolysaccharide compared with mouse splenic lymphocytes. This decreased stimulation was restored by the addition of purified T cells, but not macrophages. Nylon-adherent T cells exerted this helper activity only toward complement receptor-positive B cells (CR+B cells). whereas the helper activity of nylon-non-adherent T cells was effective only on complement receptor-negative B cells (CR-B cells). Since the helper activity of nylon-adherent T cells was completely abolished by the treatment with anti-Ia antiserum and complement but that of nylon-non-adherent T cells was not, it was assumed that Ia+T cells were helper cells for CR+B cells and Ia-T cells helper cells for CR-B cells. Moreover, these helper activities of both T-cell subsets were mediated by soluble factors, which were effective just before the onset of DNA synthesis of the corresponding B-cell subpopulations.
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PMID:The collaboration of T-cell subsets in the mitogenic stimulation of purified B-cell subpopulations. 31 20

Murine splenocytes contain two minor subpopulations of B cells, one inducible by lipopolysaccharide to convert within 2 h from IgD- to IgD+ and the other to change from IgD+ TO IgD-. These two subpopulations can be separated by density centrifugation. Their relative proportions show a marked age dependency: IgD- leads to IgD+ cells are more frequent in suckling mice, while IgD+ leads to IgD- inducible cells become predominant in mice older than 3 weeks. The age dependency observed in the relative proportions between the two cell types suggest that they are ontogenetically related as progenitor-successor. This hypothesis is corroborated by phenotype analysis of the two subsets, revealing IgD- leads to IgD+ cells as IgM+, Ia+, complement receptor- (CR-) and IgD+ leads to IgD- cells as IgM+, Ia+, CR+. Our data show that IgD and CR are expressed concomitantly during B cell differentiation. On further differentiation, induced by lipopolysaccharide, both markers are lost from the cell surface at different rates: IgD decreases significantly in a very short period (less than 2.5 h) while induction of a decline in CR requires longer culture periods (greater than 8 h). Th: loss of IgD may thus herald an early differentiation event toward antibody-producing cells.
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PMID:The ontogeny of B lymphocytes. V. Lipopolysaccharide-induced changes of IgD expression on murine B lymphocytes. 31 72

Immunosuppression was examined at 10 to 12 days following oral inoculation of 10,000 to 12,000 embryonated Ascaris suum eggs. Reduced antibody responses to sheep red cells (SRC) following systemic immunization were confirmed in CD-1 and C57Bl/6 mice. Infection alone induced antibody reactive with DNP equivalent to that observed after immunization with DNP--Ficoll. There was a decrease in thymus and spleen size by day 8 of infection, followed by a splenic proliferative response during the second week. In the second week, serum antibodies reactive with SRC, chicken erythrocytes, DNP and bacterial lipopolysaccharide were demonstrated, suggesting polyclonal B-cell stimulation. The cellular basis of immunosuppression was investigated by in vitro culture of splenocytes from C57Bl/6 mice. Differential leucocyte counts of splenocytes before culture demonstrated a relative increase in plasma cells, blastoid cells, complement receptor-bearing lymphocytes and eosinophils, with a relative decrease in small lymphocytes. The splenocytes had reduced responses to T-cell mitogens, as measured by thymidine incorporation in vitro, and reduced antibody responses to SRC and DNP--Ficoll. In vitro, cell mixing experiments did not demonstrate suppressor cells in the spleens of infected mice.
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PMID:Analysis of immunosuppression during early acute infection of mice with Ascaris suum. 70 11

Strain A/J mice made secondary indirect plaque-forming cell (PFC) responses to azobenzenearsonate (ABA) conjugates of giant keyhole limpet hemocyanin (KLH), a thymic-dependent antigen, but not to conjugates of Ficoll, a T-independent antigen. ABA-Ficoll was also unable to elicit a response in animals primed with ABA-KLH, which have an expanded anti-ABA memory cell pool. On the other hand, ABA-Ficoll rendered mice unresponsive to ABA-KLH when administered before priming or boosting with the T-dependent immunogen. Hence, the T-independent antigen was able to tolerize but unable to trigger B-memory cells responsive to the T-dependent antigen. A/J mice immunized with dinitrophenyl conjugates of Ficoll or bovine IgG (BGG) made vigorous IgM and IgG PFC responses. PFC responses to ABA-KLH and 2,4-dinitrophenyl (DNP)-BGG were abrogated by depleting mice of C3 with cobra venom factor, whereas the IgM and IgG PFC responses to DNP-Ficoll were unaffected. B lymphocytes were fractionated on the basis of receptors for C3 and the subpopulations were assayed for in vitro PFC responses to DNP-Ficoll. Very little response was obtained from complement receptor lymphocyte [CRL(+)] B cells, whereas CRL(-) cells were more responsive than unfractionated B cells. Both populations responded to a polyclonal B-cell mitogen (lipopolysaccharide). On the other hand, the in vitro PFC response to a T-dependent antigen (sheep erythrocytes) correlated with the presence of CRL(+) B cells in the cultures. However, a minor component of this response, sensitive to anti-Thy-1 serum, was made by CRL(-) B cells, indicating the existence of subpopulations of T-dependent B cells with different signalling requirements. The results suggest that most B cells responsive to T-dependent antigens possess receptors for C3 and that C3 plays an obligatory role in the response of these cells. A distinct subpopulation of B cells which lack C3 receptors respond to T-independent antigens. The precursors of PFC for the ABA epitope reside largely or exclusively in the CRL(+) compartment in A/J mice, whereas precursors for the DNP determinant are found in both compartments.
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PMID:Murine B-cell subpopulations responsive to T-dependent and T-independent antigens. 108 26

Human polymorphonuclear leukocytes (PMN) preincubated overnight with 100 U/mL gamma-interferon (IFN-gamma) had an increased metabolic response, as measured by iodination and/or superoxide production, to stimulation by tumor necrosis factor (TNF), granulocyte-macrophage colony-stimulating factor (GM-CSF), formylmethionyl-leucyl-phenylalanine (FMLP), opsonized zymosan, and lipopolysaccharide (LPS), as compared with cells comparably preincubated in the absence of IFN-gamma. The decline in the staphylocidal activity of the stored PMN was also prevented in part by IFN-gamma, as was the depressed adherence of PMN stimulated with phorbol myristate acetate (PMA), FMLP, TNF, GM-CSF, and LPS. This protective effect of IFN-gamma on PMN function was associated with the prolonged surface expression of the complement receptor three (CR3) alpha-chain (CD11b), CR3 beta-chain (CD18), FcRII (CD32), and FcRIII (CD16), and the appearance of surface FcRI (CD64). The polymerase chain reaction (PCR) was used to amplify neutrophil RNA-derived cDNA recognized by synthetic oliogonucleotides designed from published nucleotide sequences for specific proteins. Using this procedure, mRNA for gp91-phox, p67-phox, p47-phox, CD64, two forms of CD32, CD16, CD11b, CD18, and actin were found to be depressed after overnight storage of neutrophils, and this decrease in steady-state mRNA levels was in part or totally prevented by IFN-gamma. CD64 and gp91-phox mRNA were generally increased by IFN-gamma to a level greater than that of freshly isolated neutrophils. Northern analysis of CD64 and p47 phox mRNAs confirmed the findings with the PCR method. These findings suggest that storage of PMN in a functionally active state is favored by the presence of IFN-gamma.
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PMID:Effects of gamma-interferon on human neutrophils: protection from deterioration on storage. 131 36

The stimulating activity of several preparations isolated from a membrane proteoglycan of a nonencapsulated smooth strain of Klebsiella pneumoniae (Kp-MPG) on the oxidative burst of human blood monocytes was assessed by luminol-enhanced chemiluminescence (CL). Five Kp derivatives were studied: a 34-kd acylpoly(1,3)galactoside (APG), obtained by drastic alkaline hydrolysis and purified by chromatography; an APG preparation subjected to acid hydrolysis that removed the core part and all fatty acids, leaving intact the galactose chain of APG (GC-APG); an APG preparation subjected to mild oxidation (ox APG); a preparation obtained by mild alkaline hydrolysis of Kp-MPG, containing additional ester-linked C14 and C16 fatty acids bound to the APG molecule (EFA-APG); and a polymer of the latter compound, APG pol. EFA-APG directly stimulated monocyte CL, whereas Kp-MPG, APG pol, and the whole bacterial cells had little or no activity. APG itself and ox APG induced a weaker response than EFA-APG. Polymyxin B sulfate completely inhibited the CL response to bacterial lipopolysaccharide (LPS) but not to EFA-APG. The stimulating action of EFA-APG on blood monocytes was dependent on the extracellular levels of both calcium and magnesium. Preincubation of monocytes with monoclonal antibody anti-Mac-1 directed against CD11b, the alpha chain of complement receptor type 3 (CR3; CD11b/CD18), strongly inhibited CL activation by EFA-APG and to a lesser extent CL activation by unopsonized zymosan and rough LPS. Altogether, these findings provide indirect evidence for the contribution of the CD11b/CD18 integrin in the functional interaction of EFA-APG with monocyte membranes. They demonstrate the role of fatty acids in the triggering of monocyte oxidative burst, while the polysaccharide chain itself does not contribute to induction of the CL response in this model. In keeping with the effects of EFA-APG and APG, we show that the monocyte CL response was triggered by bacterial LPS from the rough strain of Salmonella minnesota Re 595 and its lipid A, but not by LPS from smooth strains, again suggesting a critical role for the lipid moiety.
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PMID:Activation of human monocyte chemiluminescence response by acylpoly(1,3)galactosides derived from Klebsiella pneumoniae. 143 64

Acute inflammation is important for defence against infection, wound repair and the mediation of auto-immune tissue destruction. Myelomonocytic recruitment in acute inflammation is a stereotyped and non-specific response to tissue insult which begins within 2 h. In this study, lipopolysaccharide was injected into the murine CNS and other body sites of mice to compare the inflammatory responses. Doses of lipopolysaccharide which induced typical myelomonocytic recruitment in skin and the choroid plexus had no effect in CNS parenchyma, apart from the morphological activation of local resident microglia. The CNS parenchymal response proceeded independently of that in the choroid plexus-cerebral ventricles and had three distinct and unique phases. Initially there was minimal neutrophil exudation and a two-day delay before any increase in macrophage-microglial cell number. Next, there was a rapid increase in macrophage-microglial cell numbers during the third day, mainly due to recruitment of blood monocytes. During this phase, leukocyte recruitment was restricted to monocytes which rapidly adopted the arborized microglial phenotype. Monocytes migrated through an intact blood-brain barrier independent of changes in solute permeability. Finally, there was a florid myelomonocytic reaction predominantly in the white matter, one week after intracerebral injection of 2 micrograms lipopolysaccharide. At this time, the leukocyte reaction disrupted the blood-brain barrier, mononuclear phagocytes expressed macrophage morphology and abundant major histocompatibility complex Class II antigen, and T lymphocytes were present. Myelomonocytic entry into the CNS was partially inhibited by prior blockade of the type 3 complement receptor, known to mediate leukocyte adhesion to endothelium elsewhere. The processes which lead to rapid myelomonocytic recruitment in other tissues are absent in CNS parenchyma. Understanding the molecular mechanisms responsible could have considerable significance both for CNS pathophysiology as well as possible anti-inflammatory therapeutic application elsewhere in the body.
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PMID:The acute inflammatory response to lipopolysaccharide in CNS parenchyma differs from that in other body tissues. 158 21


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