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

To explore mechanisms of T cell regulation governing mucosal IgA immune response, concanavalin A-induced cloned T cell lines from Peyer's patches (PP) as well as spleen were established. The cloned cell lines expressed Thy- 1.2(+), Lyt-l(+)2(-) and were radioresistant (1,500 rad). The capacity of the cloned T cells to regulate Ig synthesis was determined by measuring their effect on lipopolysaccharide (LPS)-induced polyclonal Ig synthesis by PP B cells. In initial studies Ig secreted by B cells was determined by double antibody radioimmunoassay. LPS in the absence of cloned T cells induced abundant amounts of IgM (average 8,860 ng/2 x 10(5) B cells) and IgG (average 1,190 ng/2 x 10(5) B cells), but little or no IgA. The addition of PP cloned T cells markedly suppressed production of IgM (88 percent at the highest T/B cell ratio, 4:1), but the addition of spleen cloned T cells suppressed only a little or not at all. IgG production was inhibited by both PP and spleen T clone cells (70 percent at the 4:1 T/B ratio), wheras IgA synthesis was enhanced by both clones, but only to a limited degree. In subsequent studies the expression of class-specific surface Ig (sIg) and cytoplasmic Ig (cIg) on/in unseparated PP B cells as well as Ig class- specific PP B cells and spleen B cells during culture with or without the cloned T cells was determined by immunofluorescence. The major findings were as follows: (a) Compared with unseparated B cell cultures and cultures of purified sIgM B cells derived from PP containing LPS alone, cultures containing LPS and PP cloned T cells showed a marked decrease in cIgM-, sIgG-, and cIgG-expressing cells that was accompanied by a striking increase in sIgA-bearing, but not cIgA-containing, cells. In contrast, unseparated B cell cultures and cultures of purified sIgM B cells derived from PP containing LPS and spleen cloned T cells did not show any increase in sIgA- bearing cells. (b) Compared with purified sIgG-bearing PP B cell cultures containing LPS alone, purified sIgG-bearing PP B cell cultures containing both LPS and PP cloned T cells showed no substantial change in sIgG- or cIgG- expressing cells, and no sIgA- or cIgA- expressing cells appeared. (c) Compared with sIgA-bearing PP B cell cultures containing LPS alone, purified sIgA-bearing PP B cell cultures containing both LPS and PP cloned T cells showed no increased proliferation, and cIgA cells did not occur. Cultures of purified sIgM B cells derived from spleen containing LPS and PP cloned T cells showed qualitatively similar changes. From these results we conclude that PP cloned T cells induced class-specific switching from sIgM- to sIgA- bearing B cells, whereas spleen cloned T cells lacked this property, although they may have induced an IgM {arrow} IgG or intersubclass IgG switch. These processes seem to be in part tissue dependent. Furthermore, the PP switch T cells appear to operate as true switch cells, which govern the pathway of DNA recombination events, rather than as classical helper cells, which act to expand already differentiated cells. Finally, these switch T cells probably account for the fact that PP are an important source of IgA B cells and also a major site of IgA heavy chain class switching during gut-associated mucosal B cell proliferation and differentation.
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PMID:Mechanisms regulating IgA class-specific immunoglobulin production in murine gut-associated lymphoid tissues. I. T cells derived from Peyer's patches that switch sIgM B cells to sIgA B cells in vitro. 618 11

A total of 95 K1 Escherichia coli strains of the O (lipopolysaccharide) serotypes O1, O7, or O18 had been analyzed previously for the ability to cause bacteremia after colonizing the gut of newborn rats. In this study, these strains were tested for their resistance to the bactericidal activity of rat serum. All strains that had caused bacteremia in a high percentage of the inoculated rats were able to survive for several hours in 90% adult rat serum. With only a few exceptions, O7:K1 and O18:K1 strains were serum resistant and virulent, whereas O1:K1 strains were serum sensitive and avirulent. Serum sensitivity was due to the classical complement pathway. K1 strains of all three O serotypes were resistant to the alternative complement pathway. O7:K1 and O18:K1 cells were killed efficiently after the classical pathway was triggered by specific antilipopolysaccharide antibodies. However, killing of O1:K1 bacteria by the classical pathway system did not require antibodies. Isolated O1-lipopolysaccharide fixed complement more efficiently than did isolated O7- or O18-lipopolysaccharide, suggesting that the differences in the chemical structure of the O antigens are responsible for the observed differences in complement sensitivity. In combination with epidemiological data, the results indicate that antibody-independent classical pathway activation provides an important defense mechanism for newborns against certain gram-negative infections.
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PMID:Degree of antibody-independent activation of the classical complement pathway by K1 Escherichia coli differs with O antigen type and correlates with virulence of meningitis in newborns. 619 83

The effects of breast- and bottle-feeding on serum immunoglobulin levels and specific antibody responses have been examined in 30 infants on five occasions from 6 days until 9 months of age. No significant differences were found on any sample occasion between the two feeding groups in total immunoglobulin levels of G, M and A classes or in class-specific antibody responses to tetanus toxoid vaccine. This suggests that the capacity of the two groups to make serum antibodies develops similarly. Concentrations of antibodies to commensal Escherichia coli 'O' lipopolysaccharide antigens, however, were significantly greater in the bottle-fed group, and it is suggested that this difference is due to an increase in the exposure of the systemic immune system to these gut antigens in the bottle-fed infants. There are several possible explanations for this increased exposure and the resulting effects on the infants' immune system. These experiments also illustrate a possible role of breast milk in stimulating the immune system.
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PMID:In-vivo immune responses of breast- and bottle-fed infants to tetanus toxoid antigen and to normal gut flora. 620 38

In this review, we have emphasized: 1) bacterial lipopolysaccharide (LPS) involvement in IgA responses to orally administered thymic-dependent (TD) antigens; 2) characterization of Peyer's patch (PP) lymphoreticular cells; and 3) gastrointestinal immunization with gram negative pathogens and anti-LPS immunity to infection. Gut LPS, which interacts with PP lymphoreticular cells, is a major determinant for host responses to orally administered TD antigens. Bacteroides species are the principal microflora present in the gastrointestinal tract and our studies with phenol-water LPS extracts from Bacteroides fragilis indicate that both polysaccharide and lipid A activate lymphoreticular cells. The B. fragilis lipid A moiety, like that derived from E. coli and Salmonella LPS, induces B cell mitogenic responses in cultures from LPS responsive mice, but does not stimulate C3H/ H3J B cells. The inability of lipid A to stimulate gut-associated lymphoreticular tissue (GALT) cells of C3H/HeJ mice results in the induction of greater T helper cell activity in this tissue in response to orally administered TD antigens and ultimately results in an elevated IgA response pattern. Murine PP contain accessory cells (approximately 1% dendritic cells and 6-8% macrophages) and lymphocytes T (35-38%) and B (40-42%). Recent studies with antigen-specific T cell clones from C3H/ H3J PP have resulted in the isolation of IgA isotype-specific T helper cells (PP Th A cells). PP Th A cells are antigen-specific, bear Fc alpha receptors, and require H-2 histocompatibility with B cells for helper activity. PP Th A cells most effectively collaborate with surface IgA (sIgA)-bearing B cells (IgA committed B cells) for IgA isotype responses. Other studies have shown that PP dendritic cells and T cells form clusters when stimulated in vitro with sodium periodate and that these clusters promote polyclonal IgA responses in B cell cultures. Polyclonal IgA responses in cultures containing PP cell clusters from C3H/ H3J mice are considerably higher than those in identical cultures from LPS responsive mice. In other studies, the environmental influence on GALT B cells and their resultant commitment to IgA isotype is under investigation. CBA/N, X-linked immunodeficient (xid) mice possess an immature splenic B cell population which cannot respond to thymic-independent class-2 (TI-2) or certain TD antigens. However, GALT B cells of xid mice possess a mature Lyb-5+ B cell subpopulation capable of both TI-2 and TD responses.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mucosal immunoregulation: environmental lipopolysaccharide and GALT T lymphocytes regulate the IgA response. 623 50

A soluble hemagglutinin/protease from Vibrio cholerae has been suggested to be a putative virulence factor and protective antigen. However, clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers. A gut mucosal immunoglobulin A antibody response to soluble hemagglutinin was seen in 4 of 8 Bangladeshi patients, but in 0 of 10 North American volunteers. These responses were much weaker than those to cholera toxin or lipopolysaccharide.
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PMID:Weak serum and intestinal antibody responses to Vibrio cholerae soluble hemagglutinin in cholera patients. 646 62

To determine whether a defective proliferation of gut mucosal lymphocytes is a contributory factor to the pathogenesis of inflammatory bowel disease, we assessed their reactivity toward mitogens and bacterial antigens. Spontaneous replication of intestinal lymphoid cells was higher than that of patient-matched peripheral blood lymphocytes. That gut mucosal lymphocytes appear to be activated in loco was confirmed by a striking, time-dependent increase in the number of stable E rosettes generated by culturing unstimulated Crohn's disease intestinal lymphoid cells. The responses of lymphocytes from inflamed and normal mucosa to polyclonal mitogens were not only comparable to each other, but to those of corresponding peripheral lymphocytes, as well. Peripheral blood lymphocytes from patients with Crohn's disease showed less proliferation to Bacteroides and lipopolysaccharide antigens than did those from control individuals, but replicated similarly in response to Staphylococcus aureus and the enterobacterial common antigen: In contrast, when cultured with Staphylococcus aureus or with lipopolysaccharides, but mucosal lymphocytes from Crohn's disease proliferated 3-5 times more than did those from normal mucosa, while lymphoid cells from both sources were equally stimulated by Kunin antigen. Overall, this study found no evidence for a defective proliferative capacity of immune competent cells at the gut mucosal level in inflammatory bowel disease.
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PMID:Studies on isolated gut mucosal lymphocytes in inflammatory bowel disease. Detection of activated T cells and enhanced proliferation to Staphylococcus aureus and lipopolysaccharides. 697 54

The first line of defense against pathogens that enter the host by the oral route appears to involve the gut-associated lymphoreticular tissue-e.g., Peyer's patches (PP). Although animals can readily be immunized by orally administered antigen that mobilizes the secretory immune system, there is a total lack of local antibody synthesis in the PP and the cellular basis for this deficiency remains a mystery. A lymphoreticular cell population, obtained when murine PP were treated with a neutral protease (Dispase), consisted of accessory cells [macrophages (MPhi)] and T and B lymphocytes. In vitro cultures of these PP cell preparations with the thymic-dependent antigen sheep erythrocytes (SRBC) resulted in good anti-SRBC plaque-forming cell (PFC) responses. The time courses of these responses were identical to those seen with spleen cell cultures. Submitogenic concentrations of concanavalin A (Con A) and optimal doses of N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP) and lipopolysaccharide (LPS) enhanced in vitro responses of PP cell cultures to SRBC. PP possess fully functional antigen-presenting MPhi because incubation of optimal proportions of splenic T and B cells with purified populations of PP MPhi supported good in vitro immune responses. Murine PP possess all of the necessary elements for an IgA immune response because PP cell cultures derived from mice orally primed with SRBC and immunized with SRBC in vitro gave high IgA anti-SRBC PFC responses. All of the adjuvants tested (LPS, MDP, and Con A) enhanced IgA responses in PP cell cultures from orally primed mice; however, Con A induced the greatest enhancement. These results demonstrate that murine PP possess MPhi capable of accessory cell functions for in vitro immune responses and that oral priming with antigen induces the precursor T- and B-cell populations necessary for IgA responses, that are potentiated by adjuvants, in PP cell cultures. Thus, murine PP possess the lymphoreticular cells required for antibody responses; however, the tissue architecture likely prevents local responses in vivo. The finding that enzymatically dissociated PP contain all of the necessary cellular components for antibody synthesis, whereas the in vivo tissue architecture prevents the complex interactions necessary for this response, suggests that the initial inductive events take place in situ, and additional cell interactions are required for final differentiation of IgA-synthesizing plasma cells to occur at distant mucosal sites.
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PMID:In vivo immune response to a T-cell-dependent antigen by cultures of disassociated murine Peyer's patch. 697 42

Several immunobiological properties of cell envelope components of Vibrio cholerae such as mitogenicity, antigenicity, adjuvanticity and toxicity were tested in mice. Killed whole bacteria, spheroplasts, lipopolysaccharide and outer membrane proteins possessed mitogenic activity as determined by [3H]thymidine uptake in spleen cell cultures. All these components predominantly stimulated murine bone-marrow derived (B) lymphocytes. The mitogenicity induced by V. cholerae lipopolysaccharide was similar in magnitude to that observed with Salmonella typhimurium lipopolysaccharide. Vibrio cholerae lipopolysaccharide was mitogenic for gut-associated lymphocytes such as those obtained from Peyer's patches and small intestine. Antibody formation at the cellular level was detected by the haemolytic plaque assay. Plaque-forming cells to V. cholerae lipopolysaccharide were only detected when mice were immunized intraperitoneally with intact cells or with spheroplasts. Among the various cell envelope components, lipopolysaccharide alone possessed adjuvant properties as it increased the number of plaque-forming cells to sheep erythrocytes fourfold in mouse spleens. Also, lipopolysaccharide was the only component found to be toxic for the mouse (LD50 0 . 5 mg). Neither spheroplasts nor outer membrane of V. cholerae showed adjuvanticity or toxicity in mice.
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PMID:Immunological properties of the cell envelope components of Vibrio cholerae. 701 69

An enzyme-linked immunosorbent assay was used to detect antibody to specific bacterial lipopolysaccharide (LPS) in serum and in pokeweed mitogen (PWM) stimulated culture supernatants of peripheral blood mononuclear cells from four patients with alcoholic cirrhosis (AC). Antibody to LPS (derived from a single strain of Escherichia coli isolated from each patient's stool), was detected in the sera of each patient to a 10(-4) dilution. Only one of four control sera was positive at the 10(-4) dilution, with the others positive at 10(-3) dilution. Antibody to LPS was detected in the culture supernatants in three of the four patients and in none of the control subjects. Supernatants from patient cultures pretreated with mitomycin C or harvested after 1 day of incubation did not have detectable antibody. These results indicate that we can expand, in vitro, the population of peripheral blood B lymphocytes obtained from patients with AC and cause them to synthesize antibody against specific LPS from their own gut flora.
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PMID:In vitro synthesis of antibody to specific bacterial lipopolysaccharide by peripheral blood mononuclear cells from patients with alcoholic cirrhosis. 701 48

Normal mice have large numbers of cells (PFC) making antibody to an autoantigen which is exposed when their own erythrocytes are treated with proteolytic enzymes. Antibody against this antigen can be demonstrated in serum by haemolysis tests against the treated cells; this antibody rises to high levels within 2 to 3 days after injection of E. coli lipopolysaccharide. using quantitative absorption tests we have located the 'bromelain mouse' (BrM) autoantigen in the gastrointestinal tract as well as in erythrocytes; this distribution pattern resembles that of classical blood group antigens. We have described the ontogenetic development of PFC, B cells capable of activation by LPS, serum antibody and antigen. Free antigen is found in the gut shortly after birth. B cells rise rapidly to high levels in the peritoneal cavity, but require a short period of culture to release detectable antibody. PFC and B cells increase more slowly in spleen to adult levels by 3 weeks of age. The serum antibody lags behind PFC development. The pattern is consistent with an early stimulation of B cells in the peritoneal cavity by gut-derived antigen. We discuss the possible relationship of this autoimmune response to high natural responses against other autoantigens in mice, man and other species.
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PMID:Ontogeny of the autoimmune reaction in normal mice to antigens in erythrocytes and gut. 702 Oct 25


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