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)

?The stimulatory and inhibitory effects of concanavalin A (Con A) on the in vitro primary immune responses to a T-dependent antigen, sheep erythrocytes (SRBC) and a T-independent antigen, TNP-lipopolysaccharide (TNP-LPS) have been studied. Inhibition of the response to both antigens was optimal when 2 mug Con A were added at the initiation of the culture period. The response to SRBC was considerably enhanced by the addition of Con A 24 hr later. In contrast, this late addition did not stimulate the TNP-LPS response and often inhibited it. Inhibition of the TNP-LPS response required the participation of T cells since it was not observed in cells from adult thymectomized irradiated bone marrow-reconstituted (ATXBM) mice. The response to TNP-LPS was somewhat enhanced in ATXBM cells, but the degree of enhancement was strikingly less than that observed for SRBC. LPS per se did not block the stimulatory effect of Con A on the SRBC response, and was observed to act synergistically with this lectin. None of the Con A effects observed required the participation of adherent cells. These observations are consistent with a model in which different subpopulations of T cells are responsible for the inhibitory and stimulatory effects. They further suggest that the Con A inhibitory activity acts via a T cell to inhibit directly the B cell response to antigen.
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PMID:Effects of concanavalin A on the in vitro responses of mouse spleen cells to T-dependent and T-independent antigens. 109 Jun 54

Old (6 months) overtly autoimmune female NZB X NZW F1 (B/W) mice were markedly hyporesponsive to sheep erythrocytes (SRBC). The response to SRBC was restored by a) simultaneously injecting lipopolysaccharide (LPS) with SRBC or b) transferring bone marrow and thymocytes with SRBC into lethally x-irradiated (100 R) syngeneic old recipients. The in vitro PFC response of old B/W spleen cells to SRBC was restored by adding in culture a) theta-positive and radioresistant spleen cells from old B/W mice primed with homologous antigen or b) activated T cells from the spleens of lethally x-irradiated (1000 R) old B/W mice injected with old syngeneic thymocytes and SRBC but not horse erythrocytes. Various populations of unprimed lymphoid cells from young (4 to 6 weeks) female B/W mice, which respond normally to SRBC, were not capable of restoring the response of old syngeneic mice in vitro or in vivo. These results suggest the existence of a suppressor of T cell activation and/or B and T cell interaction in old autoimmune B/W mice.
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PMID:T cell activation and cellular cooperation in autoimmune NZB/NZW F hybrid mice. 109 16

Mechanisms of nonspecific elicitation of anti-sheep erythrocyte (SRBC) hemolytic antibody plaqueforming cells (PFC) in mouse spleens with an injection of bacterial endotoxin (lipopolysaccharide (LPS)) were studied in comparison with the genesis of naturally occurring "background" PFC in normal mouse spleens and of rapidly arising PFC in mouse spleens after immunization with SRBC. The cytokinetic pattern of anti-SRBC PFC response after an injection of LPS was quite different from that of the response elicited after immunization with SRBC. In addition, even though LPS nonspecifically elicited anti-SRBC PFC response in mice, LPS could not confer any immunological memory on mouse immunocytess for a "secondary-type" anti-SRBC PFC response to restimulation with LPS or SRBC. The administration of rabbit anti-mouse thymocyte immunoglobulin or anti-SRBC antiserum in mice markedly suppressed the PFC response after immunization with SRBC, but did not do so after stimulation with LPS. Neonatally thymectomized mice could still respond to stimulation with LPS, producing anti-SRBC PFC in their spleens. Injections of actinomycin D or cyclophosphamide into mice resulted in obvious reductions of the PFC responses elicited by either LPS or SRBC. However, injections of these immunosuppressive antisera or drugs did not affect the number of anti-SRBC PFC in normal mouse spleens. These results suggest that the genesis of anti-SRBC PFC developed under different conditions, i.e., background PFC, LPS-stimulated PFC, and antigen-stimulated PFC, are quite different from each other, and that the nonspecific elicitation of anti-SRBC PFC by LPS does not require the helper function of T lymphocytes. No obvious difference, however, was observed in the time of ontogenic maturation among these three different anti-SRBC PFC in the mouse spleens judging from when they were first manifested after birth.
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PMID:Nonspecific elicitation of antibody-forming cells in the mouse spleen by bacterial lipopolysaccharide. 109 68

Immunotoxicity of the technical atrazine formulation, AAtrex, was examined in C57Bl/6 female mice following a sublethal exposure to equivalent 1/2-1.64 LD50 doses of the herbicide. Animal weight was not affected by the herbicide exposure. No dose-related changes could be concluded for fluctuations in organ weight, changes in the spleen cell number and cell viability. Furthermore, cytofluorometric studies showed no significant changes in the frequency of L3T4-positive and Lyt-2-positive T-cells. Functional in vitro assays of mitogen activation showed no marked effects of AAtrex exposure on lymphocyte stimulation by lipopolysaccharide (LPS), phytohemagglutinin (PHA) and concanavalin A (Con-A). In addition, sublethal exposure to AAtrex did not affect interleukin-2 (IL-2) production by splenic cells. Furthermore, no dose-related effect could be concluded from a transient suppression of a primary humoral IgM response to sheep erythrocytes (SRBC) as well as from a transient inhibition of a specific T-cell response to alloantigens in mixed lymphocyte reaction (MLR). Exposure to equiv. 1/2-1/16 LD50 doses augmented phagocytic activity of peritoneal macrophages, without any visible AAtrex dose-related effect. Normal humoral and cellular responses were restored at 14-40 days after the herbicide exposure. Overall, transient and reversible immunosuppression of humoral-mediated and cell-mediated responses and activated macrophage phagocytic activity could not be attributed to the direct chemical-related effect of sublethal exposure to AAtrex.
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PMID:Limited immunotoxic potential of technical formulation of the herbicide atrazine (AAtrex) in mice. 153 25

Monocrotaline (MCT) is a member of a class of naturally occurring phytotoxins known as pyrrolizidine alkaloids, and is a toxicological concern to both man and his livestock. The purpose of these studies was to evaluate the effect of a 14-day oral MCT (0-100 mg/kg per day) exposure on the functional integrity of various immunocyte effector systems in C57BL/6 mice, as well as to investigate potential mechanisms for its immunotoxicity. Decreases in lymphoid organ weights and cellularity, and resident peritoneal exudate cell (PEC) number were only observed after exposure to the highest dose of 100 mg/kg MCT. This dose also inhibited NK cell cytotoxicity, while the total number of NK lytic units per spleen was decreased (-53%) after exposure to 50 mg/kg MCT. Following i.p. injection of SRBC, the percentage of PEC macrophages containing engulfed SRBC was significantly increased in MCT-exposed mice, while the percentage of large vacuolated (activated) macrophages was decreased in a dose-dependent manner. Exposure to MCT significantly decreased the total number of Ig+ cells without altering the number of CD4+ and CD8+ cells. The antibody responses (PFC/10(6) spleen cells) to two T cell-independent antigens, TNP-LPS and DNP-Ficoll, were significantly decreased at all MCT doses, and the degree of suppression of both responses was identical at coincident doses. MCT exposure (25 mg/kg) significantly suppressed the blastogenic response to the T cell mitogen concanavalin A (-38%), and to the B cell mitogen lipopolysaccharide (-58%). These results indicate that exposure to MCT can alter the functional integrity of various immune effector responses in a dose-dependent manner, and suggest that the B cell may be a relatively more sensitive target of MCT immunotoxicity compared to T cells, macrophages and NK cells.
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PMID:Tier-2 studies on monocrotaline immunotoxicity in C57BL/6 mice. 177 39

Resident peritoneal cells were obtained from BALB/c mice and enriched for cells of the macrophage lineage by adherence onto 96 well tissue culture plates. Adherent cells were then exposed to various recombinant cytokines or supernatants from cell cultures, for 24 h. The ability of such adherent antigen presenting cells (APC) to support proliferation and development of helper function in T-lymphocyte populations, primed with sheep erythrocytes (SRBC), was examined. The addition of cytokines to the APC population did not enhance either proliferation of the T-cells nor helper function, assessed by assay of polyclonal IgG secretion in second cultures, beyond that obtained with control APC. The potent macrophage activators interferon-gamma and lipopolysaccharide caused a significant decrease in both parameters of T-cell activity. This effect was caused by a prostaglandin-mediated pathway inasmuch as indomethacin (1-5 microM) prevented it. Further analysis showed that this negative signal predominated until macrophages were diluted below 5% of the total cell population. At 0.5% macrophages, interferon-gamma stimulated APC function of these cells compared with untreated macrophages. Despite the relative difficulty in manipulating the T-cell response by attempted modulation of the APC with cytokines, the simple manoeuvre of incubation of otherwise responsive, primed T-cells with a high dose (10%) of SRBC during in vitro restimulation, caused the proliferation and helper function of these T-cells to be markedly decreased. This phenomenon was seen regardless of the cytokine used to stimulate the APC population. These studies further clarify the dual role the macrophage in regulation of T-cell responses.
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PMID:The effect of macrophage activation state on antigen presenting capability as defined by helper T-cell function. 183 40

TI-31, at concentrations of 10 and 100 microM, suppressed the antibody response to T cell-dependent (sheep red blood cells, SRBC) and -independent antigens (trinitrophenyl-lipopolysaccharide, TNP-LPS and TNP-Ficoll). The anti-SRBC response was suppressed by TI-31 when T cells were replaced by a supernatant of concanavalin A (Con A)-stimulated spleen cells, indicating the drug had influence on T lymphocytes, B lymphocytes and macrophages. TI-31 augmented the Con A-induced suppressor T cell (Ts) assessed by anti-SRBC plaque-forming cells response in vitro. The drug (10 mg/kg, p.o.) potentiated antigen specific Ts induction in vitro after injection of a high dose of SRBC. The results demonstrate that TI-31 enhanced Ts induction, which resulted in a diminution of antibody formation.
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PMID:Characterization of immunomodulating action of TI-31 on antibody response in mice. 183 1

The effects of polyclonal antibodies to mouse serum components on the primary humoral immune response of mice in vivo were studied. It was observed that rabbit IgG to complement component C3 and albumin and mouse IgG to C5, but also heat-aggregated non-immune rabbit IgG, enhanced the agglutinating antibody response to sheep erythrocytes (SRBC). Since the increase in response was only observed when antigen and antibodies were administered via the same route (i.p.), immunological adjuvant activity was implicated. Ineffectiveness of anti-C5 IgG in C5-deficient mice indicated that the antibody-induced adjuvant activity is mediated by in vivo formed immune complexes (IC). The adjuvant activity of IC was reduced by selective C3-depletion of animals, pointing to a requirement of C3. The effect of variations in other parameters was studied with anti-C3 and anti-C5 IgG as immunoadjuvant. The immunostimulatory effect was most pronounced when the antibodies were administered simultaneously with or shortly before antigen. Treatment of animals with antibodies one or two days before antigen, however, resulted in a suppression of the response. The response to thymus-independent antigens was not enhanced by anti-C3 nor by anti-C5 IgG. Optimal adjuvant activity of anti-C3 IgG was observed at low antigen doses. Nude mice were insensitive to the immunopotentiating effect of anti-C3 and so was the F1 progeny of BALB/c male and CBA/N female mice expressing a B-cell maturation defect. C5 deficiency and lipopolysaccharide (LPS) non-responsiveness did not affect the adjuvant activity of in vivo formed C3-anti-C3 IC.
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PMID:C3- and T-cell-dependent adjuvant activity of in vivo formed immune complexes. 187 75

The present study was conducted to establish baseline profiles of various macrophage functions in four commercial broiler genetic lines designated as Lines 1, 2, 3, and 4. All experiments were carried out between 2 to 3 wk of age. Total numbers of peritoneal exudate cells per bird collected 42 h after a single i.p. injection of Sephadex-G50 were comparable among the lines. Line 1 produced fewer macrophages along with reduced phagocytosis of opsonized SRBC, whereas Line 4 macrophages were depressed in unopsonized SRBC phagocytosis. Macrophages from Lines 2 and 4 killed internalized Escherichia coli earlier than macrophages from Lines 1 and 3. Supernatants from lipopolysaccharide-treated macrophages from Lines 1 and 2 exhibited significantly higher cytolytic activity against LSCC-RP9 tumor cells when compared with supernatants from Line 3 and 4 macrophages. The current study demonstrates genetic variation among the four broiler lines for mononuclear phagocytic system functions.
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PMID:Comparison of macrophage function in several commercial broiler genetic lines. 195 55

The purpose of the present study was to assess the effect of fat source on the immune response of chickens. One-day-old pullets were fed corn and soybean meal-based diets containing 7% by weight one of the following fat sources: lard, corn oil, canola oil, linseed oil (LO), or fish oil (FO). After being fed experimental diets for 3 wk, humoral and cellular immune responses were assessed. Chicks were injected with SRBC and antibody titers were measured, 7 days later, by hemagglutination. Concanavalin A (Con A), pokeweed mitogen (PWM), or lipopolysaccharide (LPS)-stimulated proliferation of splenocytes was assessed by [3H]thymidine incorporation. Results demonstrated that antibody titers in FO-fed chicks were higher (P less than .005) compared with titers in chicks fed the other fat sources. The proliferative response to Con A and PWM were 30 to 50% lower (P less than .13 and P less than .05, respectively) in chicks fed the oils rich in omega-3 fatty acids, LO and FO. The response to LPS was poor. The effect of dietary fats source on lymphocyte proliferation was completely abrogated when autologous chicken serum was excluded from the culture medium. Fat source also seemed to affect growth and feed intake of the chickens. In conclusion, dietary fat source has a significant impact on the immune response of chickens.
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PMID:Effect of dietary fat source on antibody production and lymphocyte proliferation in chickens. 204 52


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