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

Specific in vitro PFC responses to trinitrophenyl conjugated to sheep red blood cells are inhibited by chloramphenicol (CAP), thiamphenicol (TAP), and diuron (DIU) by B-cell impairment. However, both mitogenic and polyclonal response to lipopolysaccharide is not affected by CAP and TAP but severely inhibited by DIU. Similarly, contact of cultured cells for the first 24 h with CAP did not much affect the 4th-day in vitro PFC response but the same incubation with DIU reduced it by 70%. Moreover, DIU used at the same concentration provoked an important mortality of cultured cells. These differences suggest that the target mechanism of CAP and TAP differs from that of DIU.
 ...
PMID:Specification of the immune response: its suppression induced by chloramphenicol in vitro. 634 Jul 51

The presence of suppressor cells and their mediators has made it difficult to induce B cell mitogenic or immune responses in rat spleen cell cultures. In the present study, we have defined culture conditions required for induction of in vitro thymic independent (TI) immune responses in the rat. Rat spleen cell cultures support low responses to various trinitrophenyl (TNP) haptenated antigens including TNP-Brucella abortus (TNP-BA), TNP-lipopolysaccharide [LPS; either phenol (Ph)- or butanol (Bu)-water extracted], TNP-Ficoll, and TNP-dextran. However, all of these antigens induced good splenic anti-TNP PFC responses when given at appropriate doses in vivo. When spleen cells were depleted of adherent cells and cultured with TI antigens in vitro, good anti-TNP PFC responses were seen with TNP-BA, whereas, lower responses were induced by TNP-LPS (Ph or Bu). No responses were observed in cultures incubated with either TNP-Ficoll or TNP-dextran. Purified splenic B cell cultures [prepared by panning on plates coated with anti-rat F (ab')2] supported good responses to TNP-LPS (Ph or Bu) and TNP-BA. The addition of irradiated splenic adherent cells (macrophages, M phi) to either M phi-depleted or purified B cell cultures completely abrogated in vitro responses to TNP-BA or TNP-LPS (Ph or Bu). Purified splenic B cell cultures generally responded poorly to TNP-Ficoll or TNP-dextran. Addition of indomethacin (IM) to spleen cell cultures abrogated suppression and allowed anti-TNP PFC responses to TNP-BA, TNP-LPS (Ph or Bu), TNP-Ficoll, and TNP-dextran. Furthermore, nude spleen cell cultures treated with IM, also allowed significant TNP-Ficoll and TNP-dextran immune responses; however, untreated cultures did not respond to these antigens. Our studies indicate that rat splenic B cell cultures are responsive to TI antigens, and highest responses occur with the murine TI-1 class, e.g., TNP-BA and TNP-LPS. Inhibition of suppression with IM restored splenic B cell responses to the murine TI-2 class, i.e., TNP-Ficoll and TNP-dextran.
 ...
PMID:Immunoregulation in the rat: requirements for in vitro B cell responses to classical TI-1 and TI-2 antigens. 641 10

Over a wide range of concentrations affinity-purified rabbit anti-mouse mu chain antibodies, or their F(ab')2 fragments, inhibit the appearance of immunoglobulin-secreting cells (plaque-forming cells; PFC) in lipopolysaccharide-stimulated murine spleen cell cultures without affecting proliferation. Both IgM and IgG PFC are inhibited although the number of blasts bearing surface IgG remains unaltered. The IgM and IgG PFC response could be reconstituted to normal levels in cell cultures suppressed by mu-specific antibodies by the addition of supernatants from in vitro propagated helper T cell clones, or from EL4 lymphoma cells induced with phorbol ester. Interleukin 1-containing P388 supernatant, or recombinant DNA-derived murine interferon-gamma, did not reconstitute the PFC response in cell cultures suppressed by mu-specific antibodies, indicating that other factors are responsible for these effects. When spleen cell cultures, pre-activated with either lipopolysaccharide or monoclonal mouse mu-specific antibodies coupled to Sepharose, were exposed to EL4 supernatants in the presence of soluble mu-specific antibodies, maturation to secretion was inhibited while proliferation was not. The implications of these findings on assay systems for B cell growth and maturation factors are discussed.
 ...
PMID:Effects of mu-specific antibodies on B cell growth and maturation. 643 43

Adult female (C57BL/6 X C3H)F1 (B6C3F1) mice were treated with diethylstilbestrol for 14 days and assayed for the ability to produce antibody to a T-dependent antigen, a T-independent antigen, and to respond in vitro to stimulation by a polyclonal activator, bacterial lipopolysaccharide (LPS). No suppression of the in vivo antibody responses were observed. DES produced a subtle alteration in the response to the T-dependent antigen, sheep erythrocyte (sRBC), as treated groups maintained higher PFC values than vehicle groups after the peak day of the response. DES induced an enhanced response to the T-independent antigen, DNP-Ficoll. Spleen cells from DES-exposed animals were only marginally altered in their ability to produce antibody in vitro in response to LPS. Parallel experiments indicated a comparable reduction of LPS-induced blastogenesis. Serum immunoglobulin levels were determined following DES exposure, as a measure of baseline immunocompetence. DES only caused a reduction in the immunoglobulin M (IgM) isotype. DES exposure caused a significant enhancement of the activity of the reticuloendothelial (RES) system. Experiments were performed to assess the effects of enhanced RES function on concentrations of 51Cr labeled sRBC, which were optimal for antibody production. When sRBC were administered i.p., there was no effect on either the Ab response (as reported above) or on the number of sRBC localized in the spleen. In contrast, when sRBC were administered i.v., exposure to DES reduced (approximately 50%) both the Ab response and the number of sRBC localized in the spleen. Enhanced phagocytic function and alterations in antigen distribution must be considered in the interpretation of in vivo immune responses.
 ...
PMID:Effects of subchronic exposure to diethylstilbestrol on humoral immune function in adult female (C3B6)F1 mice. 653 73

Nonmarine luminous bacteria belonging to the genus Vibrio cholerae were extremely sensitive to the bactericidal activity of human serum. Luminous bacteria incubated in a medium containing serum showed a decrease in their in vivo luminescence that was directly proportional to the decrease in the viable count and was a function of the serum concentration. Both immunoglobulins and the complement system were required to exert the serum bactericidal activity. Serum lacking immunoglobulins or certain complement components, especially C3, did not affect the luminescence. The bactericidal effect of the serum on luminous bacteria was diminished by the presence of lipopolysaccharide or by pretreatment of the serum with different species of killed bacteria. As found in other systems, the bacteriolytic activity of serum was only augmented by lysozyme, but was not lysozyme dependent; although the luminous bacteria were converted into spheroplasts in serum containing 0.5 M sucrose, their in vivo luminescence was almost not affected. This system could easily distinguish between the C classical pathway and the properdin pathway. Ethylene glycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid, which inhibits only the classical complement pathway, did not inhibit the decrease in luminescence as did EDTA. Thus, it was possible to distinguish between deficiencies in complement components participating in both pathways and complement components that were involved only in the classical pathway. This system could also be used as a substitute to the hemolytic system in complement fixation tests.
 ...
PMID:Determination of serum bactericidal activity with the aid of luminous bacteria. 661 81

Splenocytes of C57BL/6J mice injected with a Trichinella spiralis larval extract for 7 consecutive days were transferred in two doses into isogenic, immunocompetent mice. On the 3rd day, some recipients were immunized with 10(9) sheep red blood cells and others were killed to investigate blastogenic response of their splenocytes to concanavalin A (Con A), Escherichia coli lipopolysaccharide (LPS), and Mycobacterium's purified protein derivative (PPD). On the 8th day of immunization, the corresponding mice were killed to study rosette-forming cells (RFC) and direct and indirect plaque-forming cells (D- and I-PFC) in their spleens. Transfer of 10(6) cells depressed the Con A reactivity and the number of RFC and 1-PFC, but increased the PPD reactivity and the number of D-PFC in the recipients, as compared to control mice receiving splenocytes from donors injected with a saline solution. Ten million cells inhibited only the Con A reactivity, but enhanced the number of LPS- and PPD-responding cells and of D-PFC in the recipients over the controls. Inoculation of cells from mice injected with bovine serum albumin did not reproduce the same effects. Splenocytes of mice treated with T. spiralis extract simultaneously inhibit and enhance diverse functions of the immune system. Stimulation is exerted on IgG antibody production and appears to be mediated by suppressor T-cells. Stimulation is exerted mainly on IgM antibody formation. Depression seems to be antigen-specific; it is partially compensated by the concurrent suppression, and it is probably a result of macrophage activation.
 ...
PMID:Responses of B-cells to mitogens and antigen in mice receiving isogenic splenocytes from animals treated with Trichinella extract. 697 Feb 60

Hydroquinone and catechol are two metabolites of benzene that are potential inducers of hematotoxicity. We investigated the in vivo toxicity of these metabolites toward the development of polyclonal, plaque-forming cells (PC-PFC) from progenitor B lymphocytes. Dextran sulfate (DxS), lipopolysaccharide (LPS), or the two mitogens combined (DxS + LPS) were used to induce proliferation and maturation of these progenitors to PC-PFC. Groups of 4 C57BL/6 mice were exposed to 2 daily doses, either intravenously or intraperitoneally, of hydroquinone (100 mg/kg) or catechol (75 mg/kg) for 3 consecutive days. Spleen and marrow cells were harvested for culture 1 day later. The results demonstrated that both metabolites were cytotoxic to spleen cells. Hydroquinone (100 mg/kg) also reduced marrow cellularity, whereas catechol (75 mg/kg) did not significantly affect marrow cellularity. Each compound reduced the frequency of PC-PFC developed from the spleens and marrows of treated mice, but only catechol selectively inhibited the maturation of LPS-activated marrow progenitors into end-stage PC-PFC. These experiments demonstrate the immunotoxic potential of hydroquinone and catechol in vivo through the reduction of progenitor B lymphocytes and suggest that inhibition of precursor cell maturation may play a significant role in the hematotoxicity observed after chronic exposure to benzene.
 ...
PMID:Hydroquinone and catechol reduce the frequency of progenitor B lymphocytes in mouse spleen and bone marrow. 697 15

Antibodies to the nuclear antigen SM are specific for systemic lupus erythematosus in humans and mice. In order to study the cellular mechanisms of anti-Sm generation, a hemolytic plaque assay to identify and enumerate lymphocytes secreting anti-Sm has been developed by using SRBC coated with purified Sm by a modified carbodiimide technique. Anti-Sm-specific PFC were found in MRL/Mp-Ipr/Ipr and MLR/Mp- +/+ mice whose sera contained anti-Sm, but were never detected in anti-Sm-negative MRL mice or in normals. Spleen cells from anti-Sm-positive MRL/Mp-Ipr/Ipr mice generated anti-Sm PFC spontaneously after 4 days of in vitro culture, whereas cells from normal mice or anti-Sm-negative MRL mice were never observed to produce spontaneous anti-Sm, even when cultured in the presence of bacterial lipopolysaccharide. The generation of anti-Sm by MRL cells in vitro was found to be dependent on the presence of T cells, but the ability of cells from individual MRL mice to generate anti-Sm appeared to be limited by the availability of Sm-specific B cell precursors and not due to a relative absence of T cells capable of providing help for the anti-Sm response. Analysis at the cellular level of the in vitro generation of a disease-specific autoantibody by using the methods described should facilitate understanding of mechanisms of autoreactivity.
 ...
PMID:Anti-Sm autoantibodies in MRL mice: in vitro detection and generation of antibody-forming cells. 698 38

The data presented in this paper show that different thymus-independent (TI) antigens have a differential capacity of inducing antibody formation in mouse bone marrow, both after primary and secondary intravenous immunization. Primary immunization with certain TI antigens (e.g., lipopolysaccharide [LPS], TNP-LPS, DNP-Ficoll) induces the appearance of antibody-forming cells not only in the spleen, but also in the bone marrow. A single injection of certain other TI antigens (e.g., pneumococci [Pn], TNP-conjugated detoxified LPS [TNP-dLPS], TNP-conjugated Brucella abortus bacteria [TNP-BA] ), on the other hand, induces antibody formation in the spleen only. After secondary immunization with these TI antigens only TNP-BA induces a PFC response in the bone marrow. Pn, TNP-dLPS and TNP-BA, but also DNP-Ficoll, are unable to induce bone marrow antibody formation after secondary injection of the antigen, in spite of the clear-cut secondary type character of the splenic response. Thus, the absence of a bone marrow PFC response after secondary immunization with these antigens is not due to a failure to induce memory B cells. This data implies that either two subpopulations of memory B cells exist, one giving rise to antibody formation in the spleen and the other accounting for the bone marrow response, or that antibody can selectively inhibit the secondary bone marrow antibody response to certain TI antigens.
 ...
PMID:Antibody formation in mouse bone marrow during secondary type responses to various thymus-independent antigens. 698 19

Normal mice have large numbers of cells (PFC) making antibody to an autoantigen which is exposed when their own erythrocytes are treated with proteolytic enzymes. Antibody against this antigen can be demonstrated in serum by haemolysis tests against the treated cells; this antibody rises to high levels within 2 to 3 days after injection of E. coli lipopolysaccharide. using quantitative absorption tests we have located the 'bromelain mouse' (BrM) autoantigen in the gastrointestinal tract as well as in erythrocytes; this distribution pattern resembles that of classical blood group antigens. We have described the ontogenetic development of PFC, B cells capable of activation by LPS, serum antibody and antigen. Free antigen is found in the gut shortly after birth. B cells rise rapidly to high levels in the peritoneal cavity, but require a short period of culture to release detectable antibody. PFC and B cells increase more slowly in spleen to adult levels by 3 weeks of age. The serum antibody lags behind PFC development. The pattern is consistent with an early stimulation of B cells in the peritoneal cavity by gut-derived antigen. We discuss the possible relationship of this autoimmune response to high natural responses against other autoantigens in mice, man and other species.
 ...
PMID:Ontogeny of the autoimmune reaction in normal mice to antigens in erythrocytes and gut. 702 Oct 25


<< Previous 1 2 3 4 5 6 Next >>