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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

The immune response at the level of individual immunocytes to the somatic lipopolysaccharide antigen derived from whole Vibrio cholerae and to the purified protein exotoxin from this organism were studied in terms of the role of T- and B-lymphocytes. By adoptive cell transfer studies with irradiated recipient mice, it was shown that normal spleen cells from normal syngeneic mice could readily transfer the capability of responding to both types of cholera antigens. However, when the spleen cells were depleted of T-cells with anti-theta serum and complement, antibody responsiveness to the LPS antigen, but not to exotoxin, could be achieved in recipients. Furthermore, by appropriate transfer of either bone marrow, thymus, or thymus-marrow cell mixtures to irradiated mice, it was shown that the response to the cholera somatic antigen was relatively independent of thymus cells, whereas the response to exotoxin required "helper" T-cells. The role of thymus and bone marrow cells in the intestinal tract in immune responses to the somatic and toxic antigens of cholera vibrios requires further investigation. Further studies should also provide additional information not only concerning the mechanism of the immune response to these antigens in terms of basic mechanisms of antibody formation, but also should provide valuable information in terms of anticholera immunity per se.
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PMID:Involvement of T- and B-lymphocytes in the immune response to the protein exotoxin and the lipopolysaccharide antigens of Vibrio cholerae. 109 72

TNP-lipopolysaccharide (TNP-LPS) is a potent T-independent antigen in vivo, inducing a TNP-PFC response in T-depleted animals. The structural integrity of the lipid A-KDO portion of the LPS carrier molecule appears to be required since the haptenated LPS from Salmonella minnesota Re595 is immunogenic whereas the haptenated derivative of base hydrolyzed LPS is not. The immune response is not associated with any of the common histocompatiblity types, but does depend on the ability of the host strain to respond to LPS. C3H/HeJ mice are not killed by low doses of LPS and give a poor PFC response to TNP-LPS. Lethality and immunogenicity are dominant responses in hybrids of C3H/HeJ and responder mice. The structural and genetic requirements for the response to TNP-LPS suggest an active role for the carrier in the immunogenicity of this T-independent antigen.
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PMID:Structural and genetic basis of the in vivo immune response to TNP-LPS. 110 Jul 25

The Freeman polysaccharide - the hapten of lipopolysaccharide - induced a blast transformation of mouse and rabbit spleen lymphocytes. The magnitude of the response in rabbit was quite similar to that obtained by lipopolysaccharide whereas in mice it was weaker. The stimulation of lymphocytes of both species did not require the presence of macrophages. Similar results were obtained with four LPS and their correspondent haptens prepared from S. typhi-murium, S. abortus-equi, S. johannesburg R+ and R-.
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PMID:Stimulation by haptenic Salmonella polysaccharides of murine and rabbit lymphocytes. 110 19

Addition of bacterial lipopolysaccharide to HSA during repeated immunization of rabbits neonatally rendered tolerant to HSA led to anti-HSA antibody formation in 4 out of 5 animals. In all 6 tolerant animals immunized with HSA alone tolerance persisted after cessation of the immunization series, as shown by non-immune elimination of 125I-HSA. On the other hand, immunization with HSA together with different doses of LPS did not increase anti-HSA antibody levels in tolerant and control chickens.
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PMID:Different effects of bacterial lipopolysaccharide on neonatal immunological tolerance to HSA in rabbits and chickens. 110 79

Brucella endotoxin differs from other gramnegative endotoxins in that it is recovered in the phenol phase rather than the aqueous phase of the Westphal hot phenol water procedure. This was the first described from this laboratory by Redfearn (1960) with phenol-killed smooth B. abortus and B. melitensis and has since been confirmed by others. Preliminary extraction of brucella cells with acetone, as called for in the original Westphal procedure, was followed by Renoux et al. (1973) who reported that the aqueous phase lacked endotoxic activity and the phenol phase had very low toxicity. In order to test the hypothesis that prior acetone extraction removes lipid A, we have repeated the Redfearn procedure with acetone extracted cells and have confirmed that the major portion of the endotoxic activity resides in the phenol phase. Acetone treatment does not remove the lipid A believed to be responsible for mouse lethality as well as necrotizing activity in guinea pig and rabbit skin. Preparations of brucella endotoxin (lipopolysaccharide) contain varying amounts of polypeptide some of which is tightly bound. The dermal response of sensitized guinea pigs to brucella LPS was shown to be a combination of reactions comprising those due to (1) innate toxicity of lipid A, (2) antibody mediated reactions due to polysaccharide portion of the molecule and (3) delayed hypersensitivity due to polypeptide portion of the molecule.
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PMID:Studies of Brucella lipopolysaccharide. 126 51

The ability of murine monoclonal antibodies (mAbs), directed to the inner core of Gram-negative bacterial lipopolysaccharide (LPS, endotoxin), to enhance complement-mediated killing of bacteria, was investigated. The mAbs were tested as present in ascitic fluid. It was found that ascites contains an factor that inhibited the activity of complement. This effect was evident in assays for complement-mediated lysis of antibody-coated Gram-negative bacteria (bacterial killing) or of opsonised red blood cells. Moreover, the amount of inhibitor was found to vary from one ascites to another and spanned a 60-fold range. Thus, in vitro or in vivo experiments where complement is known to play a determining role may yield incorrect results when ascites is used as a source of antibody; the use of ascites prepared from irrelevant antibody as a negative control does not eliminate this problem.
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PMID:Murine ascitic fluids contain varying amounts of an inhibitor that interferes with complement-mediated effector functions of monoclonal antibodies. 128 Feb 47

E3330 [(2E)-3-[5-(2,3-dimethoxy-6-methyl-1,4-benzoquinoyl)]-2-nonyl-2- propenoic acid], a novel synthesized hepatoprotective compound, has suppressive effects on tumor necrosis factor-alpha (TNF-alpha) generation from monocytes/macrophages in vitro. E3330 (1-100 microM) reduced lipopolysaccharide (LPS, 10 mg/ml or 1 microgram/ml)-induced TNF-alpha generation from rat resident and Propionibacterium acnes (P. acnes)-elicited peritoneal macrophages, rat and human monocytes, rat Kupffer cells, and splenic mononuclear cells in a concentration-dependent manner. E3330 also (1-100 microM) suppressed TNF-alpha generation stimulated with egg-albumin immune complex in rat P. acnes-elicited peritoneal macrophages. Northern blot analysis showed that LPS-induced expression of TNF-alpha messenger RNA (mRNA) in human blood monocytes was suppressed by E3330. These findings indicate that E3330 has a suppressive effect on TNF-alpha generation from monocytes/macrophages, regardless of origin or species, and this effect is based in part on the suppression of TNF-alpha mRNA expression.
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PMID:Suppressive effects of E3330, a novel quinone derivative, on tumor necrosis factor-alpha generation from monocytes and macrophages. 128 92

Endotoxin (lipopolysaccharide, LPS) has the property of inducing tolerance to its own biological effects. This phenomenon has been extensively studied in animal models but only few studies exist on the regulation in humans. Here we describe experiments designed to determine the cytokine regulation and cellular changes in humans during induction of LPS tolerance after repeated LPS injections. Intravenous administration of purified LPS Salmonella abortus equi to cancer patients induces high amounts of circulating tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-8 (IL-8), granulocyte colony-stimulating factor (G-CSF), and macrophage colony-stimulating factor (M-CSF). Repeated injections of LPS at daily intervals resulted in a marked downregulation of the cytokine response and in the case of TNF-alpha, IL-8, G-CSF, and M-CSF the cytokine response was reduced to baseline levels. In contrast, significant increases in serum IL-6 were detected up to day 5 of repeated LPS injections. Hematological changes included transient decreases in WBCs affecting granulocytes, monocytes, and lymphocytes, followed by a marked granulocytosis. The drop in WBCs remained unaltered throughout the 5 day course of repeated LPS injections whereas the granulocyte overshoot recovery diminished gradually. When PBMCs of the cancer patients were restimulated ex vivo a marked enhancement of the capacity to produce TNF-alpha, IL-113, and IL-6 occurred, which is in contrast to the decreasing TNF-alpha serum levels obtained in vivo. In parallel, a shift in monocyte subpopulations from CD14+/CD16- to CD14+/CD16+ cells was observed. The data provide evidence that different mechanisms are implicated in the cytokine downregulation following repeated LPS injections to cancer patients. Furthermore, PBMCs from LPS tolerant patients do not demonstrate a reduction in their capacity to produce cytokines.
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PMID:Endotoxin tolerance: regulation of cytokine production and cellular changes in response to endotoxin application in cancer patients. 128 77

In vitro plasma perfusion experiments were performed using small columns containing either resin or charcoal adsorbents to assess the removal of cytokines and endotoxin. 125I-labelled tumor necrosis factor-alpha (TNF-alpha; 500 pg/ml) and interleukin-6 (IL-6; 10 ng/ml) were added individually to human plasma. Over 4 hr of perfusion, Amberlite XAD-7 resin removed 32.5% +/- 3.3% (n = 5) of the initial amount of TNF-alpha and 71.4% +/- 3.8% (n = 5) of the initial amount of IL-6. DHP-1 polyhema-coated activated charcoal removed 17.2% +/- 6.2% (n = 5) of TNF-alpha and 48.5% +/- 7.4% (n = 5) of IL-6. Preliminary experiments were performed with lipopolysaccharide (LPS; 100 ng/ml) and interleukin-1 alpha (IL-1 alpha; 500 pg/ml), which showed that, over 4 hr, Amberlite XAD-7 removed 10.3% of the initial LPS and 29.1% of IL-1 alpha, whereas DHP-1 charcoal removed 23.2% of the initial LPS and 65.3% of IL-1 alpha. In vitro plasma ultrafiltration with either polysulfone or polyacrylonitrile membranes, as used clinically in haemodialysis, was performed with recirculation of plasma containing LPS or TNF-alpha. Neither of the substances was filtered to a significant degree. In conclusion, direct removal of these inflammatory mediators from the circulation of patients with multiorgan failure due to fulminant hepatic failure or sepsis would be possible by perfusion of plasma through adsorbents but not by haemodialysis.
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PMID:In vitro plasma perfusion through adsorbents and plasma ultrafiltration to remove endotoxin and cytokines. 129 81


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