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)

Sputum samples from seven patients with cystic fibrosis and chronic P. aeruginosa lung infection were investigated for immune complexes by PEG precipitation and in two different complement binding assays. All seven patients were immune complex positive. The components involved in immune complex formation were identified by SDS-PAGE and immunoblotting. We found P. aeruginosa lipopolysaccharide as a major antigen. Both core and O-specific saccharide antigens could be demonstrated. IgG and IgA were the immunoglobulins involved, with IgG2 as the dominating IgG subclass. Lipopolysaccharide has a number of biological activities and its presence in sputum may have consequences for the pathogenesis of lung disease in cystic fibrosis.
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PMID:Lipopolysaccharide is present in immune complexes isolated from sputum in patients with cystic fibrosis and chronic Pseudomonas aeruginosa lung infection. 155 93

We studied the function of submandibular lymph nodes (MLN) in the oral mucosa immune system as compared with that of inguinal lymph nodes (ILN) in the cutaneous one. Primary IgM, IgG and IgA antibody responses in MLN to sheep red blood cells (SRBC) as a model antigen given submucosally occurred more extensively than those in ILN to the antigen injected subcutaneously. Particularly, definite IgA synthesis was seen in MLN but not in ILN. This IgA synthesis was shown to be originated locally in oral submucosal lymphoid tissue or MLN but not in gut-associated lymphoid tissue (GALT). This suggested that the oral mucosal tissue including MLN acts like Peyer's patches in GALT for IgA synthesis. When mice were administered with SRBC and bacterial lipopolysaccharide (LPS) submucosally, the adjuvant effect of LPS was only observed on the capacity of MLN cells for secondary antibody response in vitro. This contrasted to the marked augmentation by LPS of both the primary antibody response in ILN and capacity for in vitro secondary antibody response of ILN cells of mice given SRBC and LPS subcutaneously. The radioactivities detected in the local lymph nodes and other tissues of mice given 51Cr labeled SRBC submucosally or subcutaneously were comparable with each other. MLN, however, contained more Ig+/B220+ B cells and less Thy1+/Ly-1+ T cells than ILN did, and the L3T4/Ly-2 ratio of T cell subpopulations in MLN was lower than that in ILN. Partially corresponding to this observation, the B cell-dependent area was developed more extensively in MLN than in ILN. This difference in cellular composition and organization might in part explain the reason why MLN and ILN display distinct modes of response and sensitivity to the action of LPS.
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PMID:Characterization of antibody responses of local lymph nodes to antigen given under the oral submucosa. 159 28

Shigella flexneri SFL124, with a deletion encompassing all, or nearly all, of the coding sequence of gene aroD was obtained after selection on a fusaric acid medium supplemented with 2,3-dihydroxybenzoic acid for tetracycline-sensitive mutants of S. flexneri SFL114 which is an aroD::Tn10 transductant. Two of 20 tetracycline-sensitive mutants tested in colony hybridization with a 32P-labelled DNA probe of approximately 1400 base pairs (comprising all except the 75 N-terminal base pairs of the coding region of gene aroD) did not hybridize. The selected mutant SFL124 is Congo-red positive, invades and shows a limited multiplication in HeLa cells and does not cause keratoconjunctivitis in guinea-pigs. It is well tolerated by Macaca fascicularis monkeys, is excreted for up to 4 days, elicits a slight inflammatory reaction in the colonic mucosa, stimulates significant secretory IgA responses in the intestine and serum IgA and IgG responses against the S. flexneri cell envelope lipopolysaccharide. The immune response conferred a complete protection against challenge with 1 x 10(11) (equivalent to a 100 LD50 dose) live S. flexneri SFL1.
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PMID:Live oral auxotrophic Shigella flexneri SFL124 vaccine with a deleted aroD gene: characterization and monkey protection studies. 159 87

Samples of serum from 125 patients with haemolytic uraemic syndrome, were screened for antibodies of the IgA and IgM classes to the lipopolysaccharide (LPS) of Escherichia coli O157:H7. By means of the techniques of ELISA and immunoblotting, 48 samples were shown to contain antibodies of the IgM class to E. coli O157 LPS, while 42 samples contained IgA antibodies to this O-antigen. Thirteen patients produced IgM but not IgA antibodies to the LPS of E. coli O157:H7. Of 42 patients with IgA antibodies to the E. coli O157 LPS, seven did not produce antibodies of the IgM class. From this study, screening patients' serum for antibodies to E. coli O157 LPS of the IgA class, in addition to those of the IgM class, a total of 55 patients were shown to be seropositive. This constituted an increase is in the sensitivity of obtaining evidence of infection by this organism by 12%.
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PMID:Improved detection of infection by Escherichia coli O157 in patients with haemolytic uraemic syndrome by means of IgA antibodies to lipopolysaccharide. 850 78

An attenuated Salmonella typhi strain has been sought as an improved oral typhoid vaccine and as a carrier of protective antigens of other pathogens to make hybrid vaccines. Ideally, such a strain would be safe and induce protective immune responses after a single oral dose. CVD 908 is a mutant of S. typhi wild-type strain Ty2 with recombinant deletions in two genes, aroC and aroD. In phase 1 testing to date, this strain has not produced febrile responses or other significant adverse reactions in adult volunteers given doses of 5 x 10(4) to 5 x 10(7) organisms with sodium bicarbonate. In addition, after just a single oral dose of 5 x 10(7) colony-forming units, this strain induced IgG seroconversion to S. typhi lipopolysaccharide in 83% of vaccinees and stimulated specific IgA-secreting gut-derived lymphocytes in 100% of vaccinees. CVD 908 is a new oral typhoid vaccine that should be further investigated as a carrier for expressing foreign antigens in recombinant vaccine constructs.
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PMID:Clinical acceptability and immunogenicity of CVD 908 Salmonella typhi vaccine strain. 160 47

Cytokines such as interleukin-5 (IL-5) and transforming growth factor beta 1 (TGF beta 1) increase IgA production by heterogeneous populations of lipopolysaccharide (LPS)-activated murine B cells. We have used IgA expressing murine B-lymphoma cells CH12.LX.C4.4F10 (4F10) to define the activity of these and other cytokines on IgA secretion at the single-cell level, membrane IgA expression, IgA polymerization and cell growth. IL-5 as well as LPS significantly increases IgA secretion of 4F10 cells, whereas TGF beta 1, a cytokine known to stimulate isotype switching to IgA among surface IgM-bearing B cells, inhibits IgA secretion. When tested alone, IL-1 beta, IL-2, IL-4, IL-6 and interferon-gamma (IFN-gamma) do not significantly alter IgA secretion. However, there is a synergistic increase in IgA secretion when 4F10 cells are co-stimulated with IL-5 and IL-4, while IFN-gamma inhibits IL-5-stimulated up-regulation of IgA secretion. In parallel with increased IgA secretion after cytokine stimulation, 4F10 cells display less membrane IgA. Increased J-chain steady-state mRNA levels after IL-5 or LPS stimulation are paralleled by increased mRNA levels for secreted IgA, but are not accompanied by alterations in the ratio of monomeric to polymeric IgA. IL-5 and LPS initially stimulated but later inhibited 4F10 cell proliferation suggesting an inverse relationship between proliferation and differentiation in this cell line. 4F10 cells are a useful model for the characterization of discrete aspects of IgA B-cell differentiation, since the secretory and membrane Ig and proliferative responses of this IgA B-cell line to cytokines and LPS appear to parallel those of freshly isolated murine B cells.
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PMID:Cytokine-induced differentiation of IgA B cells: studies using an IgA expressing B-cell lymphoma. 163 47

Ursodeoxycholic acid was recently recognized as an effective agent in the treatment of primary biliary cirrhosis. Experimental evidence supporting the usefulness of ursodeoxycholic acid as a potentially beneficial therapeutic agent for primary biliary cirrhosis has been reported from the biochemical and physiological aspects. In this study, we investigated the direct effects of ursodeoxycholic acid on immunoglobulin and cytokine production in vitro using plaque-forming cell assay and enzyme-linked immunosorbent assay. It was demonstrated that ursodeoxycholic acid suppressed the production of IgM, IgG and IgA induced by Staphylococcus aureus Cowan I in peripheral blood mononuclear cells derived from healthy subjects and patients with primary biliary cirrhosis and also in human B lymphoma cell lines. Furthermore, ursodeoxycholic acid suppressed interleukin-2 and interleukin-4 production induced by concanavalin A and interferon-gamma production induced by polyinosinic-polycytidylic acid, but it did not affect interleukin-1 and interleukin-6 production induced by lipopolysaccharide in peripheral blood mononuclear cells. In addition, ursodeoxycholic acid suppressed the concanavalin A-induced thymocyte proliferation mediated by interleukin-1. Cytotoxicity against lymphocytes was not observed at the concentrations of ursodeoxycholic acid used. These results suggest that the beneficial effect of ursodeoxycholic acid in primary biliary cirrhosis is mediated in part by immunosuppression.
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PMID:Immunomodulatory effects of ursodeoxycholic acid on immune responses. 163 44

The possible contribution of additional immunologic variables to the susceptibility of late complement component-deficient individuals to meningococcal disease has not been systematically examined in previous studies. Thus, we studied three groups of patients: (1) 24 healthy individuals, (2) 8 complement-sufficient individuals with a history of recurrent bacterial meningitis, and (3) 19 complement-deficient individuals with prior meningococcal infection. No statistical differences were noted among the three groups for the following parameters: the absolute number and the percentage of lymphocytes; CD3+, CD4+, CD8+, CD20+, and CD16+ cells; and the CD4+/CD8+ ratio. The concentration of C4 and circulating immune complexes was also similar among the groups. The concentrations of IgG, IgM, and IgA were slightly, but significantly, decreased in the complement-deficient individuals. Of interest, the coefficient of spontaneous and lipopolysaccharide-stimulated activation of neutrophils was significantly depressed in the deficient individuals. We hypothesize that the terminal complement components may participate in maximal neutrophil activation.
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PMID:Immunological evaluation of late complement component-deficient individuals. 164 49

Following a foodborne outbreak of Salmonella dysentery in a group of 79 women and 4 men, 6 individuals were found to have reactive arthritis (ReA). None of the affected individuals had the classical genetic marker HLA B27 although 2 of the 6 had CREG antigens. IgA antibodies to the lipopolysaccharide of the causative organism, Salmonella heidelberg, were found to be elevated in those patients with active ReA compared to those with inactive ReA or those who had dysentery but did not develop ReA. The lymphocyte proliferative response to both PHA and the whole S. heidelberg organism was impaired in the patients with ReA (active or inactive) compared with the non-ReA patient controls. In this predominantly female outbreak of Salmonellosis, the development of ReA lacked an association with HLA class I antigens commonly recognized.
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PMID:Immunoepidemiology of post-Salmonella reactive arthritis in a cohort of women. 164 56

The effect of sex hormones on the secretory immune system was studied in rats ooforectomized and substituted with oestradiol in permeable capsules deposited subcutaneously. Ooforectomized rats and sham-operated rats without oestradiol substitution served as controls. Two weeks after the ooforectomy the rats were immunized in the Peyer's patches with Escherichia coli O6 carrying type 1 fimbriae. Some rats were given a booster dose with the same antigen at the same site 3 weeks later. Bile and serum were taken 7 days after the last immunization. The oestradiol treatment did not influence the total level of IgA or IgG or the level of specific IgA or IgG antibodies in bile or serum. Instead there was a specific increase in biliary IgM antibodies against lipopolysaccharide (LPS) as well as a rise in the total IgM concentration in the bile in the oestradiol-treated rats. Despite this there was no difference in the biliary IgM anti-fimbrial antibody level between the different groups. The oestradiol treatment did not change the levels of total immunoglobulins or antibodies against fimbriae and LPS in serum. An oestradiol-induced increase similar to the one seen in biliary IgM anti-LPS antibodies in primary immunized animals was not seen during the secondary response in booster immunized rats. Thus it seemed as if the effect of oestradiol on the secretory immune system in the bile was mainly due to an influence on primary stimulated B-cell clones in the liver, producing IgM antibodies against a T-cell-independent antigen. The effect may be mediated through a direct action of oestradiol on the B lymphocytes.
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PMID:Effect of oestradiol on the secretory immune system in the rat: an increase in biliary IgM antibodies against a T-cell independent antigen. 168 44


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