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)

Intravenous injection of Klebsiella O3 lipopolysaccharide (LPS) into BALB/c mice induces an anaphylaxis-like shock within minutes. Using 5-hydroxytryptamine as a marker for platelets, we previously suggested that a rapid platelet accumulation in the liver and lung precedes the shock, and that a complement-dependent platelet-degradation is involved in the shock. Here, we examined (i) the effect of platelet-depletion (using an anti-platelet monoclonal antibody) on the shock and (ii) the contribution of macrophages to the platelet-accumulation in those organs. LPS-induced platelet-accumulations in the liver and lung were confirmed by immunostaining. In platelet-depleted mice, the shock was largely prevented. The number of F4/80-positive macrophages was much greater in liver than in lung, and the hepatic macrophages were largely lost in mice given clodronate-encapsulated liposomes. In mice treated with such liposomes, both the LPS-induced accumulation of platelets in the liver (but not in the lung) and the shock were largely prevented, and repopulation of hepatic macrophages restored these LPS-induced responses. These results suggest that (i) platelets are indeed involved in the shock, (ii) Kupffer cells mediate the hepatic platelet accumulation, and (iii) preventing this hepatic accumulation can largely prevent rapid shock being induced by LPS (at the dose used here).
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PMID:Involvement of Kupffer cells in lipopolysaccharide-induced rapid accumulation of platelets in the liver and the ensuing anaphylaxis-like shock in mice. 1643 70

Microbial infection is thought to modulate allergic disorders, and we previously demonstrated that not only mast cells (which release histamine), but also platelets are involved in the anaphylaxis induced in mice sensitised to ovalbumin (OVA). Here, we examined the effects of a lipopolysaccharide (LPS) from the oral bacterium Prevotella intermedia (Pi) on OVA-induced anaphylaxis. Upon intraperitoneal co-injection of Pi-LPS plus OVA into BALB/c mice, the Pi-LPS displayed a potent adjuvant effect comparable to that of alum (a standard adjuvant) in terms of its abilities to induce both anaphylactic shock and histamine-release following an antigen (OVA)-challenge. Moreover, an injection of Pi-LPS given to OVA+alum-sensitised mice shortly before an OVA-challenge augmented the shock-response. This LPS-pretreatment did not affect histamine-release, but did augment pulmonary platelet accumulation. Histamine was not by itself causal for shock-induction in sensitised mice. These results suggest that oral bacteria and/or their constituents (such as LPS) may help to sensitise the host to an antigen or exacerbate the host's allergic reactions ("aggravation effect"), probably by enhancing the platelet response to the antigen OVA.
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PMID:Oral bacterial lipopolysaccharide acts in mice to promote sensitisation to ovalbumin and to augment anaphylaxis via platelets. 1755 97

Dual specificity phosphatase DUSP1 (otherwise known as mitogen-activated phosphatase 1 or MKP-1) dephosphorylates MAPKs, particularly p38, and negatively regulates innate immunity. Recent studies have shown that the DUSP1 gene is transcriptionally up-regulated by glucocorticoids (GCs) and that the antiinflammatory action of GCs is impaired in DUSP1-/- mice. Here we show that GC-mediated dephosphorylation of ERK-1 and ERK-2 activated by IgE receptor cross-linking is unimpaired in bone marrow-derived mast cells (BMMCs) of DUSP1-/- mice. Dephosphorylation of phospho-p38 MAPK is impaired but only at early times of GC treatment. Proinflammatory cytokine and chemokine gene expression (CCL2, IL-6, TNFalpha) is still down-regulated by GCs in BMMCs from DUSP1-/- mice, suggesting a compensatory mechanism for the GC action in these mice. In both DUSP1+/+ and DUSP1-/- BMMCs, GC up-regulated the expression of several phosphatase genes (DUSP2, DUSP4, DUSP9, and PEST domain-enriched tyrosine phosphatase). DUSP1-/- mice show enhanced mast cell degranulation and are highly susceptible to anaphylaxis, but these effects are still down-regulated by GCs. GCs also repressed other inflammatory responses such as dinitrofluorobenzene-induced contact hypersensitivity and lipopolysaccharide-induced mortality in DUSP1-/- mice. Thus GC-mediated antiinflammatory action is largely independent of DUSP1.
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PMID:Dual specificity phosphatase 1 knockout mice show enhanced susceptibility to anaphylaxis but are sensitive to glucocorticoids. 1763 38

We previously reported that joint swelling, synovial thickening, and cartilage matrix depletion induced by the injection of anti-collagen monoclonal antibodies and lipopolysaccharide (LPS) in BALB/c mice are increased in the absence of inhibitory leukocyte immunoglobulin (Ig)-like receptor B4 (LILRB4; formerly gp49B1) in a neutrophil-dependent manner. Because both mast cells and neutrophils express LILRB4, we sought a mast cell requirement with mast cell-deficient mouse strains, but unexpectedly obtained full arthritis in Kit(W-sh) mice and full resistance in Kit(W/KitW-v) mice. Kit(W-sh) mice were indeed mast cell deficient as assessed by histology and the absence of IgE/mast cell-dependent passive cutaneous anaphylaxis in the ear and joint as well as passive systemic anaphylaxis. Deletion of LILRB4 in Kit(W-sh) mice exacerbated anti-collagen/LPS-induced joint swelling that was abolished by neutrophil depletion, establishing a counterregulatory role for LILRB4 in the absence of mast cells. Whereas blood neutrophil levels and LPS-elicited tissue neutrophilia were equal in Kit(W-sh) and Kit+ mice, both were impaired in Kit(W/KitW-v) mice. Although both strains are mast cell deficient and protected from IgE-mediated anaphylactic reactions, their dramatically different responses to autoantibody-mediated, neutrophil-dependent immune complex arthritis suggest that other host differences determine the extent of mast cell involvement. Thus, a conclusion for an absolute mast cell role in a pathobiologic process requires evidence from both strains.
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PMID:Mast cell deficiency in Kit(W-sh) mice does not impair antibody-mediated arthritis. 1799 92

Histamine is well known for its roles in allergic diseases and anaphylaxis through H(1)-receptor stimulation. The H(1)-receptor stimulation by histamine results in an increase in vascular permeability, vasodilatation, and stimulation of nerve terminals in primary sensory neurons, thereby accelerating the inflammatory responses. On the other hand, histamine has been demonstrated to be involved in the regulation of innate and acquired immune responses through H(2)-receptors. In a previous study with human peripheral blood mononuclear cells, we observed that histamine exerts various regulatory effects on monocyte/macrophage function. In this review, we discuss how inducible histamine protects mice from lethal hepatitis, induced by heat-killed P.acnes (1 mg, i.v.) followed by challenge with a low dose of lipopolysaccharide (1 microg), by reducing the excessive cytokine response in the liver. In addition, from in vivo studies with histidine decarboxylase knockout and H(1)-, H(2)-receptor knockout mice, the protective effect of histamine against fulminant hepatitis is shown to be elicited through H(2)-receptor stimulation.
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PMID:[Inducible histamine protects mice from hepatitis through H2-receptor stimulation]. 1823 72

It remains unclear whether lipopolysaccharide (LPS) pre-treatment, which prevents Th2-type responses via Toll-like receptor 4 (TLR4), inhibits anaphylaxis. To determine the dose-dependent effects of LPS pre-treatment on anaphylactic decreases in rectal temperature caused by ovalbumin (OVA) re-exposure in immunized mice, C3H/HeN mice were divided into vehicle/OVA (0 mg/kg LPS), L-LPS/OVA (0.5 mg/kg LPS), M-LPS/OVA (1.0 mg/kg LPS) and H-LPS/OVA (3.0 mg/kg LPS) groups. After receiving these treatments, the mice were systemically immunized with OVA. Negative control mice were not immunized with OVA (N-OVA). After measuring the serum levels of OVA-specific IgE and IgG1 antibodies, the mice were examined for changes in their rectal temperature and plasma histamine concentration after OVA re-exposure. The allergen-specific IgE and IgG1 concentrations in sera from L-LPS/OVA, M-LPS/OVA and H-LPS/OVA mice were significantly lower than those in sera from vehicle/OVA mice despite OVA immunization. However, the antibody levels in all OVA-immunized mice, with the exception of the IgG1 levels in H-LPS/OVA mice, were significantly higher than those in N-OVA mice. Interestingly, H-LPS/OVA mice were the only group that did not exhibit a decrease in rectal temperature, since the rectal temperatures in vehicle/OVA, L-LPS/OVA and M-LPS/OVA mice were significantly decreased by OVA re-exposure. Furthermore, the decrease in rectal temperature after OVA re-exposure in L-LPS/OVA mice, which did not exhibit an increase in the plasma histamine concentration, was significantly prevented by treatment with a platelet-activating factor (PAF) receptor antagonist alone. Taken together, the present results indicate that high-dose LPS pre-treatment may prevent anaphylaxis in OVA-immunized mice, and that this mechanism may depend on inhibition of the IgG-PAF pathway rather than the IgE-histamine pathway.
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PMID:High dose of lipopolysaccharide pre-treatment prevents OVA-induced anaphylactic decreases in rectal temperature in the immunized mice. 1843 80

The purpose of this study is to assess the role of nitric oxide (NO) in the intestinal lesions of passive anaphylaxis, since this experimental model resembles necrotizing enterocolitis. Sprague-Dawley rats were sensitized with IgE anti-dinitrophenol monoclonal antibody. Extravasation of protein-rich plasma and haemorrhagia were measured in the small intestine. Plasma histamine was measured to assess mast cell activation. The effect of exogenous NO on the lesions was assessed by using two structurally unrelated NO-donors: sodium nitroprusside and S-nitroso-Nacetyl-penicillamine (SNAP). An increased basal production of NO was observed in cells taken after anaphylaxis, associated with a reduced response to platelet-activating factor, interleukin 1beta, and IgE/DNP-bovine serum albumin complexes. The response to bacterial lipopolysaccharide and dibutyryl cyclic adenosine monophosphate (AMP) was enhanced 24 h after challenge, but at earlier times was not significantly different from that observed in controls. Treatment with either sodium nitroprusside or SNAP produced a significant reduction of the haemorrhagic lesions, which are a hallmark of rat anaphylaxis. The extravasation of protein-rich plasma was not influenced by NO-donors. The increase of plasma histamine elicited by the anaphylactic challenge was not influenced by SNAP treatment. NO-donors protect intestinal haemorrhagic lesions of rat anaphylaxis by a mechanism apparently independent of mast cell histamine release.
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PMID:Nitric oxide decreases intestinal haemorrhagic lesions in rat anaphylaxis independently of mast cell activation. 1847 30

There has been increasing evidence for the involvement of fatty acid-binding proteins (FABPs) in the cytokine production of macrophages and dendritic cells probably through the control of cellular lipid metabolism and signal transduction. Since mast cells (MCs) are recently shown to be involved in immune response through modification of cytokine production, it is possible that some FABPs could also be involved in the immune response of MCs. In this study, we found that epidermal-type FABP (E-FABP) was expressed in murine bone marrow-derived MCs (BMMCs). Using BMMCs from genetically E-FABP-null mutated mice, we demonstrated that E-FABP in BMMCs plays a key role in the production of TNF-alpha following lipopolysaccharide (LPS) stimulation. In the in vivo septic peritonitis model (cecal ligation and puncture model), E-FABP-null mice showed a significantly increased mortality compared to wild-type mice. However, no significant difference in antigen-induced cytokine production was observed between wild-type and E-FABP-null BMMCs, and systemic anaphylaxis was equally induced in vivo in both wild-type and E-FABP-null mice. These results suggest that E-FABP is specifically involved in the LPS-induced cytokine production of MCs, and could play a role in the host-defense against bacterial infection, possibly through regulation of TNF-alpha production.
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PMID:Fatty acid-binding protein regulates LPS-induced TNF-alpha production in mast cells. 1867 77

The anti-inflammatory activity of Chungkukjang, a Korean traditional fermented soybean food (Korean-style Natto), was examined for the first time. From the results, it was found that the ethanol extract of Chungkukjang inhibited 5-lipoxygenase from A23187-treated RBL-1 cells, reducing leukoriene production (50% inhibitory concentration = 54.1 microg/mL). However, it did not greatly affect cyclooxygenase-2-catalyzed prostaglandin E(2) and inducible nitric oxide synthase-catalyzed nitric oxide production from lipopolysaccharide-treated RAW 264.7 cells at the same concentration ranges. Since leukotrienes are intimately involved in some allergic disorders, the anti-allergic activity of Chungkukjang was further examined in animal models of passive cutaneous anaphylaxis (type I hypersensitivity) and arachidonic acid-induced ear edema, two well-known in vivo models sensitive to 5-lipoxygenase inhibitors. After oral administration for 5 consecutive days, Chungkukjang significantly reduced (27.3%) passive cutaneous anaphylaxis in rats at 400 mg/kg/day. It also showed in vivo anti-inflammatory activity against arachidonic acid-induced mouse ear edema. Therefore, it is suggested that Chungkukjang may be beneficial for several allergic conditions such as asthma and atopic dermatitis.
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PMID:Anti-inflammatory activity of the ethanol extract of Chungkukjang, Korean fermented bean: 5-lipoxygenase inhibition. 1880 Sep 4

In order to identify the active anti-inflammatory ingredient(s) in Cirsium chanroenicum (Compositae), its methanol extract and several solvent fractions were prepared; the methanol extract and the ethylacetate fraction inhibited cyclooxygenase-2 (COX-2)-mediated prostaglandin E2 (PGE2) and 5-lipoxygenase (5-LOX)-mediated leukotriene (LT) production in lipopolysaccharide-treated RAW 264.7 cells and A23187-treated rat basophilic leukemia (RBL-1) cells, respectively. Further bioactivity-guided fractionation of the ethylacetate fraction using column chromatography led to the isolation of pectolinarigenin (5,7-dihydroxy-4',6-dimethoxyflavone), along with pectolinarin [pectolinarigenin 7-rhamnosyl-(1-->6)-glucoside]. Pectolinarigenin strongly inhibited COX-2-mediated PGE2 and 5-LOX-mediated LT production at >1 microM, indicating that it is a dual inhibitor of COX-2/5-LOX. However, pectolinarigenin did not affect COX-2 expression or nuclear transcription factor (NF-kappaB) activation. In addition, in vivo studies demonstrated that oral administration of these two compounds at 20-100 mg/kg resulted in similar inhibitory activities against several animal models of inflammation/allergy: arachidonic acid-induced mouse ear edema, carrageenan-induced mouse paw edema and passive cutaneous anaphylaxis. All of these results suggest that pectolinarigenin and pectolinarin possess anti-inflammatory activity and that they may inhibit eicosanoid formation in inflammatory lesions. These activities certainly contribute to the anti-inflammatory mechanism of C. chanroenicum.
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PMID:Anti-inflammatory activity of pectolinarigenin and pectolinarin isolated from Cirsium chanroenicum. 1898 74


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