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)

Isolates from 646 consecutive Finnish Haemophilus influenzae type b (Hib) patients with systemic disease, collected before and during large-scale vaccinations with Hib conjugate vaccines, were analyzed by major outer membrane protein (OMP) subtyping, lipopolysaccharide (LPS) serotyping, and biotyping (BT). Strains with OMP-BT-LPS combinations (clones) 1-I-1 and 1c-I-1 disappeared at the same rate as the disease they were associated with. A preferential decrease in the number of isolates of clone 1-II-1 was recorded, whereas the reduction in disease caused by strains of clone 1-II-9 occurred at a lower rate than expected. The latter clone occurred mainly in the most densely populated area of Finland. Strains belonging to all the common Hib clones were isolated from the 16 infants who acquired Hib disease despite being (partially) vaccinated. Thus, Hib clones disappeared during mass vaccination with conjugate vaccines, although at different rates.
 ...
PMID:Changes in the distribution of Haemophilus influenzae type b clones associated with widespread infant vaccination in Finland. 143 Dec 51

Normal intestinal bacteria can initiate systemic disease by translocating out of the intestinal lumen to extraintestinal sites such as the mesenteric lymph nodes (MLN), liver, and spleen. To determine whether dietary essential fatty acids can affect the incidence of bacterial translocation, separate groups of mice were fed one of two diets for 8 days: an essential fatty acid-replete diet (EFA-R) containing a basal formula supplemented with arginine, yeast RNA, menhaden oil, and safflower oil, or an essential fatty acid-deficient diet (EFA-D) containing the same ingredients with the safflower oil replaced by menhaden oil. Mice were given either diet alone, diet plus 50 micrograms of intraperitoneal lipopolysaccharide (LPS), or diet plus 3 days of 4 mg of intramuscular metronidazole (MET) three times a day. (Both LPS and MET have been shown to increase the incidence of bacterial translocation to the MLN.) Within treatment groups there were no significant differences in the total numbers of viable ileal bacteria (separate quantitation of strict anaerobes, aerobic, and facultative Gram-positive results, and aerobic and facultative Gram-negative results). The incidence of bacterial translocation to the MLN was increased in mice fed EFA-D as compared with EFA-R in mice treated with diet alone (17% vs 0%; p less than .005) and in mice treated with diet plus LPS (71% vs 48%; p = .027). There was no difference in the incidence of bacterial translocation in mice fed EFA-D or EFA-R and treated with MET (83% vs 81%).
 ...
PMID:Effect of a diet deficient in essential fatty acids on the translocation of intestinal bacteria. 155 5

Systemic lupus erythematosus is a multifactorial systemic disease in which genetic, immunologic, hormonal, and environmental factors may contribute to disease pathogenesis. Bacterial products (eg, bacterial lipopolysaccharide [LPS]) induce a lupuslike disease in normal mice and trigger an early and accelerated form of lupus nephritis in NZB/W mice. To investigate whether the mechanism by which LPS accelerates nephritis in the NZB/W mice involves interference with processing of immune complexes (IC), we administered LPS to NZB/W mice for 5 weeks and probed the kinetics of removal, liver uptake, and organ localization of a subsaturating dose of radiolabeled IC (2.5 mg of bovine serum albumin-antibovine serum albumin). Control NZB/W mice received vehicle (saline) alone. In NZB/W exposed to LPS, features of polyclonal B-cell activation (PBA) were enhanced, anti-DNA antibodies were raised, and a proliferative glomerulonephritis developed that was associated with renal insufficiency and substantial proteinuria. This LPS-accelerated nephritis could not be attributed to altered complement concentration, to altered blood cell carrier function, to delayed removal of pathogenic (large-sized) ICs from the circulation, to impaired liver uptake of ICs, or to enhanced localization of ICs in kidney. The findings indicate that transformation of nephritis is probably the result of LPS-induced PBA, that defective processing of pathogenic IC is not a contributory factor to nephritis, and that mechanisms other than passive renal localization of circulating ICs must be operative.
 ...
PMID:Bacterial lipopolysaccharide transforms mesangial into proliferative lupus nephritis without interfering with processing of pathogenic immune complexes in NZB/W mice. 222 Oct 21

Based on a 10-year retrospective and a 15-month prospective analysis, White Mountain Apache Indian children younger than 5 years were found to have an annual incidence of Haemophilus influenzae meningitis of 254 cases/100,000--an 8-fold higher incidence than that seen in the general United States population. In our prospective surveillance, H. influenzae isolates from cases of systemic disease were further characterized by capsular type, biotype and by outer membrane protein (OMP) and lipopolysaccharide (LPS) patterns on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Unexpectedly, H. influenzae type a strains were isolated in 3/18 cases of systemic disease. All other disease-producing strains were type b. H. influenzae b strains possessing common OMP, LPS, capsular and biotype characteristics were isolated from individuals in geographically distinct communities within the reservation. These apparently identical strains were isolated from different individuals who had systemic infections that occurred months apart (longest interval, 14 months). Both OMP and LPS subtyping were necessary to discriminate among invasive H. influenzae isolates.
 ...
PMID:Haemophilus influenzae disease in the White Mountain Apaches: molecular epidemiology of a high risk population. 633 45

Circulating proinflammatory mediators have not been found in studies on typhoid fever, although the patients suffer from a systemic disease with characteristic protracted fever. The 14-kDa group II extracellular phospholipase A2 (PLA2) is induced by interleukin-1 and tumor necrosis factor and may mediate some of the effects of these cytokines. Circulating PLA2 concentrations were measured in 12 typhoid fever patients on various days after admission and after recovery. On admission, mean concentrations of PLA2 were elevated (1444 +/- 1560 ng/mL) and decreased gradually and significantly to day 14 (55 +/- 48 ng/mL). patients with complicated disease had significantly higher PLA2 levels on admission. PLA2 was not produced in a lipopolysaccharide-stimulated whole blood culture, indicating that PLA2 originates from other types of cells. These data indicate that PLA2 may be a mediator of disease in protracted inflammatory diseases such as thyroid fever.
 ...
PMID:Phospholipase A2 is a circulating mediator in typhoid fever. 779 37

The regulatory effect of endogenously synthesized eicosanoid metabolites on the expression of tissue inhibitor of metalloproteinases (TIMP), interstitial collagenase, and 92-kDa gelatinase by human macrophages was examined. TIMP and metalloproteinase production were stimulated with three agonists that produce distinct patterns of eicosanoid synthesis: lipopolysaccharide (10 micrograms/ml), denatured collagen (10 micrograms/ml), or zymosan (1 mg/ml). Indomethacin (3 micrograms/ml) or MK886 (3 microM), a specific inhibitor of 5-lipoxygenase, was used to examine the role of endogenous metabolites of arachidonic acid. Regardless of the agonist used, TIMP production by macrophages was inhibited 65% by indomethacin, synthesis of interstitial collagenase was reduced 70%, and expression of 92-kDa gelatinase was decreased 40%. In contrast, inhibition of leukotriene synthesis had no effect on metalloproteinase or TIMP production. The agonist-stimulated increase in TIMP and collagenase production was directly correlated to the cumulative prostaglandin E2 level induced by the agonist used. However, if response to an agonist was poor, the exogenous addition of prostaglandin E2 could not increase TIMP or collagenase production more than twofold, indicating an important permissive effect of the agonist on the regulation of each protein's expression. The mechanism of indomethacin inhibition of TIMP and collagenase production was studied by labeling the cells with [35S]-methionine and performing immunoprecipitation using specific antiserum. Indomethacin markedly inhibited the lipopolysaccharide-induced biosynthesis of both TIMP and collagenase. Northern analysis revealed parallel suppression of TIMP and collagenase steady-state mRNA levels by indomethacin, indicating pretranslational control. The regulation of inflammatory-cell TIMP and interstitial collagenase expression by prostaglandin E2 suggests that therapy inhibiting the cellular response to prostaglandins may be useful in cutaneous and systemic disease states involving macrophage-mediated connective-tissue destruction.
 ...
PMID:Agonist-induced expression of tissue inhibitor of metalloproteinases and metalloproteinases by human macrophages is regulated by endogenous prostaglandin E2 synthesis. 779 41

A newly defined clinical syndrome, haemorrhagic cellulitis, is described in 12 patients. The syndrome consists of an acute onset of extremely painful erythema affecting dependent areas, followed by dermal haemorrhage and sloughing of the overlying epidermis, and requiring both antibiotics and systemic corticosteroids for complete resolution. The patients usually have demonstrable Gram-negative or Gram-positive infection, of non-cutaneous origin, and underlying systemic disease. Vacuolopathic necrosis of epidermal keratinocytes, and damaged vascular endothelium of the dermal blood vessels can be demonstrated by light and electron microscopy, as well as by lectin studies. Immunocytochemical studies reveal the presence of activated macrophages and T lymphocytes. We believe the syndrome is due to lipopolysaccharide-induced or bacterial mitogen-induced tumour necrosis factor-alpha (TNF-alpha), secreted by previously primed activated macrophages in a second-set response. TNF-alpha characteristically injures endothelial cells and epidermal keratinocytes. It is thought to induce its cytotoxic effects partly via neutrophil degranulation, and partly via DNAase activation, with resultant DNA fragmentation and cell lysis. Corticosteroids have been shown not only to inhibit TNF-alpha secretion by activated macrophages, but also to block its cytotoxicity, thus accounting for the extremely rapid clinical response to this drug in conjunction with adequate and appropriate antibiotic therapy.
 ...
PMID:Haemorrhagic cellulitis: a syndrome associated with tumour necrosis factor-alpha. 830 20

We have undertaken a study to investigate the contribution of the htrB gene to the virulence of pathogenic Salmonella typhimurium. An htrB::mini-Tn10 mutation from Escherichia coli was transferred by transduction to the mouse-virulent strain S. typhimurium SL1344 to create an htrB mutant. The S. typhimurium htrB mutant was inoculated into mice and found to be severely limited in its ability to colonize organs of the lymphatic system and to cause systemic disease in mice. A variety of experiments were performed to determine the possible reasons for this loss of virulence. Serum killing assays revealed that the S. typhimurium htrB mutant was as resistant to killing by complement as the wild-type strain. However, macrophage survival assays revealed that the S. typhimurium htrB mutant was more sensitive to the intracellular environment of murine macrophages than the wild-type strain. In addition, the bioactivity of the lipopolysaccharide (LPS) of the htrB mutant was reduced compared to that of the LPS from the parent strain as measured by both a Limulus amoebocyte lysate endotoxin quantitation assay and a tumor necrosis factor alpha bioassay. These results indicate that the htrB gene plays a role in the virulence of S. typhimurium.
 ...
PMID:Study of the role of the htrB gene in Salmonella typhimurium virulence. 935 64

In addition to the commonly reported ocular signs, Chlamydia psittaci infection of kittens resulted in fever, lethargy, lameness and reduction in weight gain following ocular instillation of virulent organisms. The appearance of these systemic signs was late with respect to the appearance of ocular symptoms and occurred simultaneously with increasing levels of chlamydia-specific IgG. Measurement of acute phase reactants and IL-6 in plasma indicated that both became elevated concurrent with or slightly after the appearance of fever and remained elevated after the fever began to resolve. Preliminary data also indicated that infectious C. psittaci was present in the blood stream during this time period. The results of ocular instillation of three different levels of C. psittaci (10(3.8), 10(2.8) and 10(1.5) TCID50) indicated that the frequency of infection and the severity of ocular signs were diminished in the group receiving the lowest dose. However, the magnitude of systemic disease was similar in all animals which exhibited clinical signs, irrespective of the dose administered. The immune response to infection included elementary body (EB)-specific lymphocyte proliferation as well as the development of EB-specific IgG and IgM antibodies. The predominant antibody response was to a 45 kDa protein, the major outer membrane protein (MOMP), lipopolysaccharide (LPS), a 58 kDa doublet and 32 and 16-19 kDa proteins.
 ...
PMID:Characterization of the systemic disease and ocular signs induced by experimental infection with Chlamydia psittaci in cats. 955 58

Human granulocytic ehrlichiosis (HGE) is an emerging febrile systemic disease caused by the HGE agent, an obligatory intracellular bacterium of granulocytes. The pathogenicity- and immunity-related mechanisms of HGE are unknown. In this study, several cytokines generated in human peripheral blood leukocytes (PBLs) incubated with the HGE agent or a recombinant 44-kDa major surface protein (rP44) of the HGE agent were examined by reverse transcription-PCR and a capture enzyme-linked immunosorbent assay. The HGE agent induced expression of interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and IL-6 mRNAs and proteins in PBLs in a dose-dependent manner to levels as high as those resulting from Escherichia coli lipopolysaccharide stimulation. The kinetics of induction of these three cytokines in PBLs by rP44 and by the HGE agent were similar. Proteinase K treatment of the HGE agent or rP44 eliminated the ability to induce these three cytokines. Induction of these cytokine mRNAs was not dependent on superoxide generation. These results suggest that P44 proteins have a major role in inducing the production of proinflammatory cytokines by PBLs. Expression of IL-8, IL-10, gamma interferon, transforming growth factor beta, and IL-2 mRNAs in response to the HGE agent was not remarkable. Among PBLs, neutrophils and lymphocytes expressed IL-1beta mRNA but not TNF-alpha or IL-6 mRNA in response to the HGE agent, whereas monocytes expressed all three of these cytokine mRNAs. These observations suggest that induction of proinflammatory-cytokine gene expression by the major outer membrane protein of the HGE agent in monocytes, which are not the primary host cells of the HGE agent, contributes to HGE pathogenesis and immunomodulation.
 ...
PMID:Expression of interleukin-1beta, tumor necrosis factor alpha, and interleukin-6 in human peripheral blood leukocytes exposed to human granulocytic ehrlichiosis agent or recombinant major surface protein P44. 1081 90


1 2 3 Next >>