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)

We investigated the significance of cytokines (soluble interleukin-2 receptor, granulocyte-macrophage colony-stimulating factor, interleukin-6, and interferon-gamma) and CD68-positive microparticles in immune thrombocytopenic purpura. Cytokines were measured by enzyme-linked immunosorbent assay and microparticles were detected by flow cytometry. CD68 expression by histiocytic U937 cells incubated with lipopolysaccharide or cytokines was also assessed in a control study. The level of CD68-positive microparticles was significantly higher in the patients with thrombocytopenia than in normal controls (p < 0.01). The soluble interleukin-2 receptor level was also significantly higher in patients than in controls (p < 0.01), but the other cytokines did not show a significant difference. However, patients with severe thrombocytopenia (platelet count > 20,000/microliters) had significantly higher levels of granulocyte-macrophage colony-stimulating factor and interleukin-6 than the controls (p < 0.05). When opsonized platelets were incubated with activated U937 cells, lipopolysaccharide and granulocyte-macrophage colony-stimulating factor caused an increase of CD68-positive microparticles in the supernatant. These results suggest that granulocyte-macrophage colony-stimulating factor is released by activated T cells in immune thrombocytopenic purpura and activates monocyte/macrophage phagocytosis, resulting in an increase of circulating CD68-positive microparticles and enhanced platelet destruction.
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PMID:Significance of cytokines and CD68-positive microparticles in immune thrombocytopenic purpura. 761 50

Plasma tissue factor (TF) antigen can be detected in healthy volunteers and may be significantly increased in patients with disseminated intravascular coagulation (DIC). Plasma TF antigen level in patients with DIC was significantly reduced after therapy. The TF activity of human umbilical vein endothelial cells (HUVEC) cultured with lipopolysaccharide (LPS), cytokines and the medium of cultured mononuclear cells (MNC) was significantly increased. TF expression was induced in HUVEC and MNC by incubation with lipoproteins, suggesting that hyperlipidaemia is a direct risk factor in thrombotic disease. TF activity in HUVEC was significantly increased in the presence of plasma and this activation was higher in patients with thrombotic thrombocytopenic purpura (TTP) and DIC. Enhanced TF production by endothelial cells may be important in the pathogenesis of thrombotic diseases.
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PMID:Tissue factor expression in endothelial cells in health and disease. 764 17

Functions of B cells from (NZW x BXSB)F1 (W/BF1) mice are investigated. The W/BF1 mouse, which is an animal model for systemic lupus erythematosus (SLE) and immune thrombocytopenic purpura (ITP), produces anti-DNA and anti-platelet antibodies; W/BF1 mice show hypergammaglobulinemia (particularly increases in IgG2a and IgG2b). The ratio of small resting B cells to large activated B cells in W/BF1 mice is low compared to normal mice, suggesting that B cells in W/BF1 mice are already activated in vivo. Furthermore, small resting B cells separated by a Percoll density gradient technique show hyper-responsiveness to lipopolysaccharide (LPS) or anti-mu plus IL-4. This suggests that B cells in W/BF1 mice are genetically programmed to be easily activated, resulting in the overproduction of autoantibodies. A significant number of CD5+ B cells are found in the lymph nodes of old W/BF1 mice. These findings indicate that all cells in the B cell lineage of W/BF1 mice are already activated in vivo.
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PMID:Functional analyses of B cells in (NZW x BXSB) F1 mice. 769 97

The frequency of Shiga toxin-producing Escherichia coli (STEC) serotypes associated with postdiarrheal hemolytic uremic syndrome (HUS) cases among children and adults in the United States and the proportion with IgM or IgG lipopolysaccharide antibodies to E. coli O157 were determined by use of a nationwide sample from January 1987 through December 1991. Among 83 patients, STEC were isolated from 30 (43%) of 70 whose stool cultures yielded bacterial growth (25 E. coli O157 isolates and 5 non-O157 STEC isolates). Fifty-three (80%) of 66 patients with serum samples had positive O157 lipopolysaccharide antibody titers. Of the 83 patients, 60 (72%) had evidence of STEC infection, including 6 of 8 adults whose illnesses also met criteria for thrombotic thrombocytopenic purpura. Data from a subset of patients suggest that E. coli O157 was the cause of > or = 80% of the STEC infections. All 3 women who were postpartum had evidence of E. coli O157 infection. STEC infection should be considered the likely cause for all persons with postdiarrheal HUS.
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PMID:The United States National Prospective Hemolytic Uremic Syndrome Study: microbiologic, serologic, clinical, and epidemiologic findings. 1149 73

The term hemolytic uremic syndrome (HUS) was first introduced to describe a heterogeneous group of diseases characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Substantial progress has been made in our understanding of the etiology and pathogenesis of HUS. This article reviews some of the classic and new concepts related to the pathogenesis of Shiga toxin (Stx)-HUS and discusses their clinical relevance for the diagnosis and treatment of this syndrome. Infection with Stx-producing bacteria can induce HUS after a prodromal illness with or without diarrhea. Stx-induced renal endothelial injury is the primary pathogenic event. However, Stx also damages mesangial cells, as well as glomerular and renal tubular epithelial cells. Young children are at greatest risk for Stx-HUS because they express high levels of Stx receptors in renal glomeruli. Older children and adults express lower levels of glomerular Stx receptors and may develop Stx-HUS whenever the combined effects of lipopolysaccharide and cytokines upregulate the expression of Stx receptors and sensitize glomerular endothelial cells to Stx-induced injury, activate the coagulation-fibrinolytic system, and induce endothelial injury. Chemokine receptors and cytokines released by inflammatory cells (i.e., monocyte chemoattractant protein-1, interleukin-6, interleukin-8,) or injured endothelial cells (i.e., basic fibrobast growth factor) may play roles in this process. Measurement of the activity of a von Willebrand factor protease in plasma may help distinguish patients with thrombotic thrombocytopenic purpura from those with Stx-HUS.
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PMID:Pathogenesis of Shiga toxin-induced hemolytic uremic syndrome. 1237 20

In Thailand, no reports are available on Escherichia coli serotype O157:H7, a causative agent of severe bloody diarrhoea, sometimes associated with haemolytic-uraemic syndrome and thrombotic thrombocytopenic purpura. The reason for the non-identification of infection due to E. coli O157 in this country and in other developing countries has not been rigorously discussed. The aim of this study was to determine the humoral response against the infectious organism. The IgM and IgG antibody responses against E. coli O157 lipopolysaccharide were studied using indirect enzyme-linked immunosorbent assay. Three hundred and thirty-two serum samples obtained from healthy blood donors and patients with diseases unrelated to diarrhoea were investigated. With a cut-off value of mean +2 SDs for each age-group, the frequency of the IgM and IgG responses to O157 lipopolysaccharide was 11.74% (39 of 332 samples) and 22.59% (75 of 332 samples) respectively. Furthermore, agglutination test of 173 subjects revealed titres ranging from 10 to 40 in all the samples. The results suggest possible exposure of the Thai population to cross-reacting antigens from other intestinal organisms in addition to infection due to E. coli O157:H7.
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PMID:Antibodies among healthy population of developing countries against enterohaemorrhagic Escherichia coli O157:H7. 1659

The pathogenesis of very severe thrombocytopenia in bacterial endocarditis is uncertain. We report a 50-year-old male with platelet counts < 10 x 10(9)/l and fragmentation hemolysis complicating Staphylococcus epidermidis pacemaker endocarditis with a giant vegetation. Antibiotics, corticosteroids, high-dose intravenous gammaglobulin, and plasmapheresis (for initially-suspected thrombotic thrombocytopenic purpura) failed to produce significant platelet count increase. However, therapeutic-dose heparin anticoagulation was associated with a platelet count increase from <10 to approximately 40 x 10(9)/l, with parallel reduction in thrombin-antithrombin complexes (from 8.9 to 3.5 microg/l), facilitating surgical intervention. The thrombocytopenia promptly resolved following surgical removal of the vegetation. Culture supernatant from S. epidermidis isolated from the patient's blood induced monocytes to express procoagulant activity (assessed by factor Xa generation) equivalent to lipopolysaccharide (1 microg/ml), with half-maximal activation seen with culture supernatant diluted to 1:12,800. These data are consistent with previous animal models of endocarditis demonstrating staphylococci-induced procoagulant changes in monocytes. This case demonstrates that heparin anticoagulation can be therapeutic in infective endocarditis-associated severe thrombocytopenia in a non-bleeding patient, and that such therapy may ameliorate the platelet count enough to permit surgical intervention.
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PMID:Very severe thrombocytopenia and fragmentation hemolysis mimicking thrombotic thrombocytopenic purpura associated with a giant intracardiac vegetation infected with Staphylococcus epidermidis: role of monocyte procoagulant activity induced by bacterial supernatant. 1716 Sep 89

Exacerbation of antibody-mediated thrombocytopenia following infection with viruses has recently been demonstrated in a mouse model of the disease. The phenomenon was caused by an increased activation of phagocytes through gamma-interferon secretion in response to infection. Endotoxins from Gram-negative bacteria are also known to be potent activators of phagocytic cells. The objective of the present work was to determine whether lipopolysaccharide (LPS) could exacerbate antibody-mediated thrombocytopenia in vivo and so alter the therapeutic efficacy of intravenous immunoglobulin (IVIg), using a mouse model of thrombocytopenia. Very low doses of LPS (picogram range) and of anti-platelet antibodies (nanogram range), which did not induce thrombocytopenia individually, could synergize in vivo, resulting in significant decreases in platelet counts. The therapeutic efficacy of IVIg in antibody-mediated thrombocytopenia was significantly reduced in presence of LPS. These in vivo observations further support a role for bacterial infections in the aetiology of immune thrombocytopenic purpura (ITP) and may contribute to better understand the recognized lack of efficacy of IVIg in a significant proportion of patients with ITP.
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PMID:Picogram doses of lipopolysaccharide exacerbate antibody-mediated thrombocytopenia and reduce the therapeutic efficacy of intravenous immunoglobulin in mice. 1789 6

Helicobacter pylori infection is implicated in the pathogenesis of extradigestive diseases such as acne rosacea and idiopathic chronic urticaria and autoimmune diseases such as autoimmune gastric atrophy, rheumatoid arthritis, anti phospholipid antibody syndrome, autoimmune thyroiditis, Sjoegren syndrome, Henoch-Schoenlein purpura, and Type B insulin resistance syndrome. H. pylori eradication ameliorated the condition in some, but not all, of those with these autoimmune diseases. Recent studies primarily in Italy and Japan found that H. pylori eradication in those infected with chronic immune thrombocytopenic purpura (ITP) results in a persistent platelet count increase in over half of those treated, suggesting that although pathogenetic mechanisms underlying the relationship between H. pylori infection and autoimmune disease remain unclear, yet-unknown immunological events induced by H. pylori infection almost certainly occur in the development of autoimmune response. A majority of isolated H. pylori strains express human Lewis (Le(x) and/or Le(y) determinants and in some strains, Le(a), Le(b), sialyl-Le(x)), and H determinants in the O-chain of the surface lipopolysaccharide. Previous studies showed that this molecular mimicry helps the bacterium evade host responses while evoking autoantibody responses to Le antigens. The anti-Le(y) autoantibody is also reported to promote H. pylori adhesion to gastric epithelial cells, leading to development of gastric atrophy. Moreover, one can hypothesize that anti-Le autoreactive antibodies induced by H. pylori infection are involved in the development of autoimmune diseases, although no clinical studies showing that anti-Le immune responses are involved in the etiology of these autoimmune diseases have been conducted. Proving this hypothesis would require quantitative and qualitative analysis of autoantibodies and T cell functions to Le antigens. High frequent phase variation of Le structures in the O-polysaccharide of H. pylori may influence the immune response of patients to Le antigens.
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PMID:[Helicobacter pylori infection and autoimmune disease such as immune thrombocytopenic purpura]. 2017 6