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 effects of the beta-adrenoceptor agonist isoproterenol (ISO) and the alpha- and beta-adrenoceptor agonist norepinephrine (NE) on murine B-cell activation. Cells were stimulated either by anti-mouse mu-chain antibodies (anti-mu), or by lipopolysaccharide (LPS), or a membrane proteoglycan of Klebsiella pneumoniae (Kp MPG), a T-independent polyclonal activator distinct from LPS, which induces B-cell proliferation and Ig synthesis. ISO and NE enhanced LPS- and Kp MPG-induced B-cell proliferation and maturation into IgM-, IgG- and IgA-secreting cells. The enhancement was prevented by prior addition of the beta-adrenoceptor antagonist propranolol but not by the alpha-adrenoceptor antagonist phentolamine. Earlier events in the LPS- and Kp MPG-stimulated B-cell activation, such as increases in Ia antigen expression and RNA synthesis, were not modified by the catecholamines. Unlike ISO and NE, the membrane-permeant cyclic adenosine 3',5'-monophosphate (cAMP) analogue dibutyryl cAMP (dbcAMP), and the potent adenylate cyclase activator forskolin did not enhance but even inhibited DNA synthesis and Ig secretion stimulated by LPS and Kp MPG. In addition, ISO and NE did not enhance but strongly inhibited anti-mu-induced B-cell proliferation, and these effects were mimicked by dbcAMP and forskolin. Collectively, the data demonstrate that beta-agonists differently modulate B-cell activation depending upon the polyclonal activator, and provide additional evidence for distinct biochemical mechanisms of B-cell activation by anti-mu and LPS. Moreover, our results indicate that beta-adrenergic stimulation up-regulates B-cell responses to LPS and Kp MPG by a novel and cAMP-independent pathway.
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PMID:Differential regulation of mouse B-cell activation by beta-adrenoceptor stimulation depending on type of mitogens. 215 73

The mucosal immune system plays an important role in blocking the penetration of invasive organisms into various mucosal surfaces. Evidence now suggests neuroendocrine peptide hormones have immunomodulatory properties, including the ability to alter mucosal immunity. The potential for opioid compounds and corticotropic hormone (ACTH) to modulate mucosal immune function was investigated. We have found beta-endorphin, ACTH, and naltrindole (delta-class opioid receptor antagonist) to significantly suppress concanavalin A-stimulated Peyer's patch lymphocyte immunoglobulin production of IgA, IgG, and IgM isotypes. Oxymorphindole, a delta class opioid receptor agonist, significantly decreased IgM but not IgA or IgG production by the mitogen-stimulated Peyer's patch lymphocytes. Both oxymorphindole and naltrindole modestly reduced interleukin-2 receptor expression of concanavalin A- (Con A)-stimulated splenic and Peyer's patch lymphocytes. Neither compound appreciably affected immunoglobulin production by lipopolysaccharide-stimulated Peyer's patch lymphocytes. Collectively, these results indicate stress-related peptides such as ACTH and opioids may be involved in the regulation of immunoglobulin synthesis by Peyer's patch lymphocytes.
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PMID:Differential effect of opioids on immunoglobulin production by lymphocytes isolated from Peyer's patches and spleen. 217 75

In an attempt to vaccinate young weaned rabbits against life-threatening enterocolitis caused by Escherichia coli of the O103 serogroup, 32 New Zealand male rabbits were divided into three groups. One group remained unvaccinated as a control (Group C), and each of the other groups received one of two types of vaccine prepared with E. coli strain O103/10 cultured either in trypticase-soy broth (Group A) or in Minca agar (Group B). Bacteria were killed by formalin and administered per os for 10 consecutive days after weaning at a daily dose of 4 X 10(9) organisms. Six days after the last administration, all the animals were challenged with 1 X 10(4) virulent E. coli O103/10 and the experimental infection was monitored for 26 days. All rabbits in Group A were protected from symptoms of disease and remained alive, whereas two rabbits in Group B developed clinical signs and one died. Protection did not correlate with local or general responses to lipopolysaccharide (LPS) O103, as judged by measurement of anti-LPS O103 IgA in faeces or serum, or by serum agglutinating antibodies. Numbers of E. coli and E. coli O103 were significantly lower in vaccinated animals of Group A as compared with animals of the control group. The differences between both vaccine regimens may be partially explained by a different expression of the adhesins of strain O103/10, depending on the medium used to prepare the vaccine.
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PMID:Protection of weaned rabbits against experimental Escherichia coli O103 intestinal infection by oral formalin-killed vaccine. 218 Feb 3

The isotypic immune response of 16 individuals who developed Q fever pneumonia following exposure to an infected parturient cat was studied. The enzyme-linked immunosorbent (ELISA) test was used to detect IgM, IgA, and IgG antibodies to phase I and phase II Coxiella burnetii whole-cell antigens and to the phase I lipopolysaccharide. The indirect immunofluorescent antibody (IFA) test was also used to detect antibodies to phase I and phase II whole cells. None of the 16 subjects developed antibodies to the phase I lipopolysaccharide. The ELISA was more sensitive than the IFA test. IgM antibodies to phase II antigen were detectable by ELISA in 80% of the subjects at the time of onset of symptoms and were still present in 7 of the 8 tested at 32 weeks following the onset of symptoms. In all instances (ELISA: IgG, IgM; IFA: IgG, IgM) phase II antibodies developed earlier and reached higher levels than did phase I antibodies. The absence of antibodies to phase I lipopolysaccharide in acute Q fever combined with our unpublished findings of antibodies to phase I lipopolysaccharide in chronic Q fever suggests that this test may be used to distinguish acute from chronic Q fever.
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PMID:The immune response in a cat-related outbreak of Q fever as measured by the indirect immunofluorescence test and the enzyme-linked immunosorbent assay. 219 85

Peripheral blood B-lymphocyte markers and functions were observed in 21 patients with IgA nephropathy (IgA NP), 18 patients with systemic lupus erythematosus (SLE) and 16 controls. IgA NP B-lymphocytes similarly to that of SLE B-lymphocytes expressed significantly higher positivity with Leu 1 (CD 5) monoclonal antibody than controls. CD 5 positive B-lymphocytes are thought to be a distinct subset of the B-cells (autoregulatory B-lymphocytes) inducible in IgA NP by lipopolysaccharide (LPS) stimulation in parallel to their expression of surface IgM heavy chain positivity. The activated state of IgA NP B-lymphocytes have been proved by their higher OKIa (HLA-DR) positivities but lower IOB1a (CD 21, C3b-receptor) and decreased IgG-Fc-receptor (ox- rosette) expression. IgA NP B-lymphocytes showed a higher IgA but also IgG and IgM polyclonal immunoglobulin production than control B-lymphocytes in co-cultures with T-lymphocytes. Not only regulatory T-lymphocyte subsets but also serum derived from IgA NP patients stimulated the immunoglobulin production of IgA NP B-lymphocytes.
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PMID:[Markers of peripheral B lymphocytes and their function in IgA nephropathy]. 220 18

Recently, we have characterized a lymphocyte blastogenesis inhibitory factor (LBIF) which was purified from the culture supernatant of a human histiocytic lymphoma U-937 (Sugimura, K. et al., Eur. J. Immunol. 1989. 19: 1357). In this study, we investigated the effect of LBIF on the antibody production of autoimmune MRL mice in vitro. We demonstrated here that (a) LBIF inhibited the IgM, IgG and IgA antibody responses of lipopolysaccharide (LPS)-stimulated spleen cells of normal BALB/c mice, (b) in the case of old autoimmune MRL/Mp-lpr/lpr (MRL/l) and MRL/Mp-(+)/+ mice, however, LBIF inhibited IgM and IgA but not IgG responses of LPS-stimulated spleen cells, (c) the antibody production of all IgG subclasses, IgG3, IgG1, IgG2b and IgG2a, was not sensitive to LBIF inhibitory activity in these autoimmune mice, (d) in young MRL mice (3-5-week-old MRL/l), which were phenotypically normal, LPS-induced antibody production of all isotypes (IgM, IgG and IgA) was strongly inhibited by LBIF as shown in normal BALB/c mice and (e) in the case of 7-week-old MRL/l the insensitivity to LBIF was concomitant with the appearance of gamma + B lymphocytes. Thus, by employing LBIF as a probe, this study showed a correlation between the pathogenesis of MRL autoimmune disease and the lack of LBIF sensitivity of hyperactive B lymphocytes and suggested that the intrinsic abnormality of autoimmune MRL B lymphocytes might be confined to gamma- but not mu- or alpha-committed B cells.
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PMID:Abnormal behavior of gamma-committed B lymphocytes probed by a lymphocyte blastogenesis inhibitory factor in autoimmune MRL mice. 220 96

Enzyme-immunoassays using lipopolysaccharide as antigen were developed for the detection of bovine IgG1, IgG2 or IgA Brucella antibodies (Ab) in milk. The results of these tests were compared with those of the milk ring test (MRT) by analyzing 3212 bulk milk samples from farms located in regions where brucellosis is prevalent. Among the 105 herds detected by ELISA and/or MRT, 29 infected herds were detected by ELISA only. The 40 MRT-positive herds were also ELISA positive. Five herds became infected during the study and were detected by ELISA 15 days to 6 months prior to detection by MRT. The ELISA IgG1 titration (IgG1 ELISA) detected 92.8% of the herds found positive in the three ELISA assays. The concomitant use of IgA ELISA raised the sensitivity to 100% but slightly decreased the specificity. The IgG2 ELISA did not improve the diagnosis. The sensitivity of MRT and IgG1 ELISA was compared by testing successive dilutions in negative milk of 110 individual MRT positive milks samples. On average, IgG1 ELISA was 22 times more sensitive than MRT.
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PMID:Diagnosis of bovine brucellosis by enzyme immunoassay of milk. 221 67

The effects of age and dietary restriction on immune response were investigated using an animal model of accelerated senescence (senescence accelerated mouse, SAM). The experimental groups consisted of control (ad libitum fed) and restricted groups (fed 60% of energy intake of the controls). Spleen weight and total number of splenic cells were significantly lower in the food-restricted group at 8 mo of age. Percentages of T (Thy-1.1+) and B (surface Ig+) cells in the splenic cells were not significantly different between the two groups. The number of direct hemolytic plaque-forming cells per 10(6) spleen cells 4 d following immunization with sheep red blood cells and dinitrophenyl-Ficoll was significantly greater in the 8-mo-old mice in the food-restricted group than in the control group. In the latter group, antibody responses Progressively decreased with age. Mitogen responses to concanavalin A and lipopolysaccharide were maintained in the food-restricted group but were depressed in the control group at 8 mo. In addition, though autoantibody to single-stranded DNA increased in the control group with advancing age, there was a steady decrease in the food-restricted group until 8 mo. Serum immunoglobulin (IgA and IgM) concentrations were significantly lower in the food-restricted group than in controls at 8 mo of age. Therefore, our results suggest that when senescence accelerated mice are subjected to food restriction, there may be a modulatory effect on the immune dysfunction associated with advancing age.
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PMID:Effects of dietary restriction on age-related immune dysfunction in the senescence accelerated mouse (SAM). 223 Oct 28

In a field trial conducted in Bangladesh, ingestion of either B subunit-killed whole cell (BS-WC) or killed whole cell (WC) oral cholera vaccines by mothers was associated with a 47% reduction of the risk of cholera in their non-vaccinated children aged under 36 months. Because vaccine-induced breast-milk immunity seemed a possible explanation for these findings, we evaluated anti-lipopolysaccharide (LPS) and anti-cholera toxin (CT) IgA antibody responses in breast milk collected during the trial from 53 lactating women who ingested three doses of BS-WC, WC, or an Escherichia coli K12 strain (K12). Despite induction of moderate vibriocidal (1.4 to 2.0-fold) and anti-CT (4.5-fold) serum antibody responses, the vaccines did not elicit significant rises of anti-LPS or anti-CT IgA breast-milk antibodies. The failure of the vaccines to elicit significant levels of breast-milk anti-cholera antibodies suggests an alternative explanation for protection of young children by maternal vaccination, such as interruption of maternal-child transmission of Vibrio cholerae 01.
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PMID:Field trial of oral cholera vaccines in Bangladesh: evaluation of anti-bacterial and anti-toxic breast-milk immunity in response to ingestion of the vaccines. 225 73

Anti-2,4,6-trinitrophenyl (TNP) IgE antibody response was elicited by stimulating TNP-keyhole limpet hemocyanin-primed murine spleen cells with the same antigen in vitro. The released anti-TNP IgE was assayed by antigen- and isotype-specific enzyme immunoassay developed in our laboratory. When prostaglandin E2 (PGE2) was added to the lymphocyte culture at 10(-7) M, anti-TNP IgE response was augmented two- to fourfold. Interestingly, PGE2 did not affect the production of anti-TNP antibodies belonging to other isotypes including IgM, IgG1, IgG2a, IgG2b, IgG3 and IgA. Moreover, PGE2 showed neither enhancing nor interleukin 4-replacing activities in the polyclonal IgE response by B cells stimulated with lipopolysaccharide and interleukin 4. When endogenous prostaglandin synthesis was inhibited by 10(-6) M indomethacin, the anti-TNP IgE response, but not the corresponding IgG response, was suppressed by 30%-60%. These results suggest a potential role of PGE2 in the up-regulation of the antigen-specific IgE response.
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PMID:Prostaglandin E2 as a selective stimulator of antigen-specific IgE response in murine lymphocytes. 225 88


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