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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunity to bacterial infection involves the joint effort of the innate and adaptive immune systems. The innate immune response is triggered when the body senses bacterial components, such as lipopolysaccharide, that alarm the body of the invader. An array of cell types function in the innate response. These cells are rapidly recruited to the infection site and activated to optimally perform their functions. The adaptive immune response follows the innate response, and one cell type in particular, dendritic cells (DCs), are the critical link between the innate and adaptive responses. This review will summarize recent data concerning the events that occur early during oral infection with the intracellular pathogen Salmonella, with emphasis on the phagocytic cells involved in combating the infection in the gut-associated lymphoid tissues. In particular, recent findings concerning the recruitment and activation of mononuclear phagocyte populations and dendritic cell subsets will be presented after an overview of the Salmonella infection model.
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PMID:Monocyte and dendritic cell recruitment and activation during oral Salmonella infection. 1772 Feb 54

An indirect ELISA using soluble whole cell antigen was used to screen serum samples obtained from breeder and layer flocks some of which had shown clinical or bacteriological evidence of infection with Salmonella Gallinarum or S. Pullorum. There was good correlation between Salmonella infection and the presence of serum samples showing high optical density (OD) values. Sera from seven flocks showing high values were retested using group D (0-1, 9, 12) lipopolysaccharide (LPS) and g,m-H flagella as detecting antigens. Sera from six flocks produced high OD values with LPS and low values with flagella confirming infection with a non-flagellate, group D Salmonella while one produced high values with both antigens indicating mixed infection with another group D serotype.
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PMID:Examination by ELISA of sera obtained from chicken breeder and layer flocks showing evidence of fowl typhoid or pullorum disease. 1864 98

The aspartate-specific cysteine protease caspase-1 is activated by the inflammasomes and is responsible for the proteolytic maturation of the cytokines IL-1 beta and IL-18 during infection and inflammation. To discover new caspase-1 substrates, we made use of a proteome-wide gel-free differential peptide sorting methodology that allows unambiguous localization of the processing site in addition to identification of the substrate. Of the 1022 proteins that were identified, 20 were found to be specifically cleaved after Asp in the setup incubated with recombinant caspase-1. Interestingly, caspase-7 emerged as one of the identified caspase-1 substrates. Moreover half of the other identified cleavage events occurred at sites closely resembling the consensus caspase-7 recognition sequence DEVD, suggesting caspase-1-mediated activation of endogenous caspase-7 in this setup. Consistently recombinant caspase-1 cleaved caspase-7 at the canonical activation sites Asp(23) and Asp(198), and recombinant caspase-7 processed a subset of the identified substrates. In vivo, caspase-7 activation was observed in conditions known to induce activation of caspase-1, including Salmonella infection and microbial stimuli combined with ATP. Interestingly Salmonella- and lipopolysaccharide + ATP-induced activation of caspase-7 was abolished in macrophages deficient in caspase-1, the pattern recognition receptors Ipaf and Cryopyrin, and the inflammasome adaptor ASC, demonstrating an upstream role for the caspase-1 inflammasomes in caspase-7 activation in vivo. In contrast, caspase-1 and the inflammasomes were not required for caspase-3 activation. In conclusion, we identified 20 new substrates activated downstream of caspase-1 and validated caspase-1-mediated caspase-7 activation in vitro and in knock-out macrophages. These results demonstrate for the first time the existence of a nucleotide binding and oligomerization domain-like receptor/caspase-1/caspase-7 cascade and the existence of distinct activation mechanisms for caspase-3 and -7 in response to microbial stimuli and bacterial infection.
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PMID:Targeted peptidecentric proteomics reveals caspase-7 as a substrate of the caspase-1 inflammasomes. 1866 12

In Germany now, the recognition of Salmonella infections in pig herds is based on three different commercial tests detecting antibodies against Salmonella-derived lipopolysaccharide (LPS). However, a serious disadvantage of these tests, used so far, is the restricted detection of antibodies belonging predominantly to the immunoglobulin class g (IgG). Therefore, a new test was developed to detect three Ig classes (IgM, IgG and IgA). Different constellations between the three Ig classes allow the evaluation of the current infection status of each pig. Under field conditions, this was proved in three different vaccination trials using a commercial Salmonella Typhimurium live vaccine.
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PMID:[Antibody response after immunization with a Salmonella Typhimurium live vaccine in dependence on the way of application]. 1882 4

Salmonella enterica subspecies I serotypes are responsible for the vast majority of salmonellosis in mammals and birds, yet only a few factors specific to this group that allow them to persist in this niche have been identified. We show that STM0557, a S. enterica subspecies I-specific gene encoding an inner membrane protein, is critical for faecal shedding and intestinal persistence of S. enterica serotype Typhimurium ATCC14028 in Salmonella-resistant mice, but mutations in this gene do not diminish short-term intestinal colonization or invasion of cultured epithelial cells. STM0557 and two neighbouring genes, located on a pathogenicity island termed SPI-16, resemble genes of the gtrA,B, gtr(type) cluster in seroconverting bacteriophages. In general, the gtr genes encode proteins responsible for serotype conversion of the infected bacterium by addition glucose residues to repeating O-antigen subunits of lipopolysaccharide (LPS). In lysogenized Shigella, such modifications have been previously shown to be constitutively expressed and to facilitate invasion of host cells. We show that serotype Typhimurium gtr orthologues, STM0557-0559, are responsible for 'form variation' or glucosylation of the O12 antigen galactose (4 position) to generate the 12-2 variant. Form variation in Typhimurium is not constitutive, but occurred upon exposure and during intracellular growth of serotype Typhimurium in J774 macrophages. Our data suggest that the 12-2 antigen is a S. enterica subspecies I-specific LPS modification that enhances long-term intestinal colonization, and is in contrast to the role of O-antigen variation described for Shigella.
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PMID:'Form variation' of the O12 antigen is critical for persistence of Salmonella Typhimurium in the murine intestine. 1882 10

Salmonella Enteritidis is still a major cause of human food borne infections and can be associated with the consumption of meat and chicken eggs. It is the world's most common cause of salmonellosis in part because it has the ability to colonize the oviduct and contaminate eggs. It was shown that when stored at room temperature, S. Enteritidis bacteria can multiply extensively in contaminated eggs. Using the in vivo expression technology, it was shown that the rfbH gene, involved in lipopolysaccharide O-antigen synthesis, is transcriptionally induced during growth in whole eggs at room temperature. A S. Enteritidis DeltarfbH strain was unable to multiply in eggs at room temperature and did not survive in egg white at 42 degrees C. The attenuation was most likely caused by an increased susceptibility of the DeltarfbH mutant to yet undefined antibacterial components of the egg albumen.
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PMID:The Salmonella Enteritidis lipopolysaccharide biosynthesis gene rfbH is required for survival in egg albumen. 1899 Jan 94

Salmonella enterica serovar Typhimurium (S. Typhimurium) infection causes an inflammatory response through activation of Toll-like receptor 4 by lipopolysaccharide. Dexamethasone, a glucocorticoid analogue, suppresses inflammatory responses by many mechanisms including inhibition of the lipopolysaccharide-induced production of proinflammatory mediators. There is little information on the effect of glucocorticoids on murine salmonellosis. In this study, we treated susceptible BALB/c mice by subcutaneous implantation of slow-release dexamethasone pellets before infection with S. Typhimurium. Dexamethasone promotes bacterial growth early in infection and induces a dose-dependent increase in bacterial growth within mouse livers and spleens. The bacterial load in organs from infected placebo-treated mice was lower than that in dexamethasone-treated mice. Glucocorticoids inhibit lipopolysaccharide-induced inflammation partially through the steroid-inducible protein annexin-A1 (ANXA1). Infection of wild-type and ANXA1 knock-out mice with S. Typhimurium led to similar organ bacterial loads. ANXA1 also did not affect the bacterial load in organs from infected dexamethasone-treated mice. This suggests that glucocorticoids, independently of ANXA1, accelerate S. Typhimurium growth in vivo in susceptible BALB/c mice.
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PMID:Dexamethasone modulates Salmonella enterica serovar Typhimurium infection in vivo independently of the glucocorticoid-inducible protein annexin-A1. 1904 46

When administered to mice at doses of 100microg/mouse and 200microg/mouse, thioridazine (TDZ) significantly protected animals from the lethality produced by a virulent strain of Salmonella enterica serovar Typhimurium and reduced the number of bacteria retrieved from the spleen, liver and heart blood. The protection conferred by TDZ against a virulent Salmonella infection is hypothesised to be due to a reduction in the 55kDa virulence protein of the outer membrane of the organism, as this protein is almost totally absent when the organism is exposed to the phenothiazine. It is further hypothesised that the reduction in the 55kDa virulence factor renders the organism susceptible to the action of hydrolytic enzymes of the neutrophil phagolysosome, whereas in the absence of exposure to TDZ intracellular ingestion and localisation of the phagocytosed bacterium does not result in killing owing to rapid induction of the two-step PmrA/B regulon that results in the eventual synthesis and insertion of lipid A into the nascent lipopolysaccharide layer of the outer membrane.
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PMID:Thioridazine protects the mouse from a virulent infection by Salmonella enterica serovar Typhimurium 74. 2000 79

Attenuated bacteria have long been developed as vaccine candidates but can have some disadvantages, such as the potential for damage to immune organs due to insufficient clearance. To minimize these disadvantages, we generated Salmonella enterica serovar Typhimurium mutants SHJ2104 (asd::cm) and HTSaYA (wzy::km, asd::cm). The wzy gene codes for the O-antigen polymerase, which is involved in lipopolysaccharide (LPS) biosynthesis, and asd codes for aspartate beta-semialdehyde dehydrogenase, which participates in cell wall formation. The strains synthesized LPS with a short-chain length, and showed lower cytotoxicity and reduced intracellular proliferation in animal cells compared to wild-type bacteria. After oral infection, the mutants were cleared in immune tissues, including the Peyer's patch, mesenteric lymph node, and spleen, within 5 days. The LD50 of the mutants in Balb/c mice was estimated to be 10(6) higher than wild-type bacteria when administered either via an oral or i.p. route, indicating that the two strains are highly attenuated. To compare the immune response to and protective effects of the mutants against wild-type bacterial infection, we inoculated the mutants into mice via an oral (1x10(10)CFU) or i.p. (1x10(7) CFU) route once or twice at a two week interval. All immune responses, such as serum IgG and secretory IgA levels, cytokine production, and delayed hypersensitivity, were highly induced by two rounds of immunization. HTSaYA and SHJ2104 induced similar immune responses, and mice immunized with HTSaYA or SHJ2104 via an i.p. route were protected against wild-type Salmonella infection even at 100-fold of the LD(50) (5x10(6) CFU). Taken together, these data indicate that HTSaYA and SHJ2104 could be developed as live attenuated Salmonella vaccine candidates.
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PMID:Immunological responses induced by asd and wzy/asd mutant strains of Salmonella enterica serovar Typhimurium in BALB/c mice. 2079 91

The main mediator of the lipopolysaccharide (LPS) response in macrophages is activation of Toll-like receptor 4 (TLR4). This generates interferon-beta (INF-beta) production that stimulates increased expression of the RNA editing enzyme ADAR1. To determine if there is an increase in RNA editing in mature miRNA in response to TLR4 activation upon Salmonella infection of macrophages we analyzed small RNA deep sequencing data. Interestingly, we found that direct infection of macrophage cell lines with Salmonella does not result in an increase of edited mature miRNA. Thus, despite elevated levels of ADAR1 during TLR4 activation of macrophages mediated by Salmonella infection, ADAR1 does not result in redirection of miRNA. The most common consequence of ADAR activity on miRNA is a reduction in the mature miRNA level due to interference with miRNA processing of pri-miRNA. However, we found very few miRNAs with reductions in level, and no significant difference between miRNAs previously reported to be edited and those reported to be not edited. In particular, we did not see significant decrease in mir-22 and mir-142, nor editing of pri-mir-22 or pri-mir-142 in infected RAW macrophages. Thus, ADAR1 has very little, if any, effect on the miRNA machinery following TL4 activation by Salmonella infection.
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PMID:Analysis of A to I editing of miRNA in macrophages exposed to Salmonella. 2103 24


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