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

The inheritance of responsiveness to lipopolysaccharide (LPS), and of a marker recognized in LPS-reactive cells by a heterologous antiserum, was studied in crosses between C3H/HeJ (nonresponder) and C3H/Tif (high responder) mice. F1 hybrid mice show codominant expression of these traits: (a) LPS-reactive cells are only hlaf as frequent in the hybrids as in the high responder parent; (b) the serologically defined marker is expressed in half as many cells in the hybrids as in the high responder parent. In backcross generations, both LPS responsiveness and this serological marker segregated into high, intermediate, and nonresponders. LPS or free lipid A, but not two other B cell mitogens (lipoprotein, and purified protein derivative of tuberculin), compete with the antiserum for binding to the B cell surface membrane, and are capable of completely inhibiting such binding without interfering with the binding of a-ti-Ig antibodies or complexes to Fc receptors. The addition of an IgG fraction of the antiserum to B cell cultures results in exponetial growth of the cells and in maturation to antibody secretion. This mitogenic activity is dose-depedent and absorbable on spleen cells from LPS high responder mice. Taken together, these observations suggest that this antiserum contains antibodies to the lipid A-specific triggering receptor on B lymphocytes.
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PMID:Genetic and functional characterization of an antiserum to the lipid A-specific triggering receptor on murine B lymphocytes. 30 50

The frequency of mitogen-reactive B cells yielding an IgG plaque-forming cell (PFC) response has been determined in vitro by limiting dilution analysis under culture conditions which allow every growth-induced B cell to grow and mature into a clone of Ig-secreting cells. The frequencies of lipopolysaccharide (LPS)-and lipoprotein-reactive precursors for IgG-secreting cells in the spleen of 6--8 wk old C3H/Tif and of C57BL/67 mice were found to be between 1 in 30 and 1 in 40 B cells and, therefore, only one tenth of the frequencies of mitogen-reactive precursors of clones secreting IgM. All IgG-secreting cells developed by switching in clones which previously contained IgM-secreting cells. This was shown in two experiments where the total number of mitogen-reactive precursor yielding IgM-secreting cell clones was limited such that 82 or 90% of all responding cultures originated from one precursor. Thus, of 480 cultures in the first and 720 cultures in the second experiment, 86 and 98 cultures were found positive, yielding IgM-secreting cells at day 5. When the same cultures were assayed at day 7 for IgG-secreting cells 9 and 10 cultures were found positive. All 19 cultures with IgG-secreting cells previously had contained IgM-secreting cells. The probability that IgG-secreting cells and IgM-secreting cells would have arisen from independent precursors can be calculated using Fisher's exact test of independence. For the two experiments those probabilities are 3.4 X 10(-7) and 4.0 X 10(-9). Since we have previously shown that each cell in a mitogen-stimulated, growing B-cell clone divides, and that each dividing cell secretes Ig, we conclude from these experiments that the large majority--in our experiments all--of the IgG-secreting cells in mitogen-stimulated B-cell clones develop by switch from IgM-secreting cells. IgG-secreting cells develop either early or late during growth of a single IgM-secreting cell clone. The switch to IgG secretion, therefore, is not fixed in the time of clonal growth after mitogenic stimulation.
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PMID:The switch from IgM to IgG secretion in single mitogen-stimulated B-cell clones. 30 89

One of three splenic B cells of 2- to 3-mo-old C57BL/6J or C3H/Tif mice are activated either by lipopolysaccharide (LPS) or by lipoprotein (LP) to grow and to mature to IgM-secreting cells. When mitogen-activated blast cells, after a 2-d activation period, are separated from nonactivated, small cells by velocity sedimentation, and no mitogen is readded, the blasts do not continue to grow but do continue to secrete IgM for several days. When the homologous mitogen is added for restimulation, the blast cells continue for several days to divide every 18 h and to develop IgM-secreting, plaque-forming cells. Frequency analyses at limiting dilutions of reactive B-blasts show that one cell in approximately equal to 1.2--1.5 blasts continue to grow and mature in the presence of the homologous mitogen, either LPS or LP. When the B-cell blasts obtained in a first activation period with either LPS or LP are restimulated with a heterologous mitogen, LPS, LP, Nocardia mitogen or mitogens contained in fetal calf serum a high proportion of the blasts continue to grow and mature to IgM-secreting cells. Frequency analyses show for LPS- or LP-blasts, restimulated in a heterologous fashion with either LP or LPS, that one cell in 1.35--1.5 blasts continue to divide and to mature to IgM-secreting cells. C3H/HeJ-splenic B-cells, which are LPS nonresponders, can only be activated to blast cells by LP. These LP-activated blasts can be restimulated by the homologous LP and by Nocardia mitogen and mitogens of fetal calf serum, but not by LPS. The results indicate that the majority of splenic B cells of 2- to 3-mo-old C57BL/6J or C3H/Tif mice are reactive to more than one B-cell mitogen. B cells, therefore, can possess in their surface membrane multireactive mitogen-receptor complexes which regulate growth and maturation.
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PMID:Mitogen-activated B-cell blasts reactive to more than one mitogen. 31 8

Splenic lymphocytes from CBA/J, AKR/A/J, BALB/c/A, C57/BL/6J, C3H/HeJ and C3H/Tif nu/nu mice and B lymphocyte or T lymphocyte preparations derived from CBA/J mouse spleen were cultivated in the presence of either concanavalin A, phytohemagglutinin, Salmonella minnesota R595 lipopolysaccharide or Proteus mirabilis soluble lipoprotein. The mitogens stimulated the incorporation of [14C]galactose into acid-insoluble cell material with the same specificity for B or T cells as that known for thymidine incorporation. The glycolipids extracted from mitogen-activated, carbohydrate-labelled B or T cells were compared by thin-layer chromatography and characteristic differences between B and T cells were noted in the ganglioside as well as in the neutral glycolipid fractions. In addition, subsets of B or T cells, namely lipopolysaccharide-responsive or lipoprotein-responsive B-cell populations or nylon-purified T cells may be recognized by characteristic neutral glycolipid bands.
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PMID:Metabolic carbohydrate-labelling of glycolipids from mouse splenocytes. Mitogen-stimulated B and T cells show different labelling patterns. 31 79

The frequency of normal murine B lymphocytes initiating growth in diluted suspension cultures in the presence of a B cell mitogen, such as lipopolysaccharide, can be increased approximately 10(4) fold by the addition of 2 X 10(6) normal thymus cells per ml. This increase in the frequency of growing cells by thymus cells can also be observed with X63-AG8 myeloma tumor cells secreting IgG1. Thus thymus cells may not contribute growth-stimulating factors, but may supply growth-supporting factors. Culture medium and plastic dishes can be conditioned by preincubation with thymus cells for a day after which the thymus cells may be omitted from further culture for maximal B cell growth. Irradiation of thymus cell abolishes their growth-enhancing properties. Thymus cells can be syngeneic and allogeneic with the growing B cells. The frequency of growing LPS-reactive, normal B cells in spleen of 6-8 week old C3H/Tif mice was determined by limiting dilution analysis to be one of three splenic B cells. With this limiting dilution analysis, it was also shown that the cloning efficiency of XB3-AG8 myeloma tumor cells in suspension culture in the presence of thymus cells is practically 100%. Analysis of the growth kinetics of single clones of LPS-reactive, normal B cells shown that these B cells divide every 18 hr. Within the first 126 hr of growth, every B cell in the clone divides, and every dividing B cell in this clone secretes sufficient immonoglobulin to form a hemolytic plaque. The conditions of in vitro suspension cultures of murine B lymphocytes are therefore perfect to the extent that every B cell capable of growth will grow as a single clone.
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PMID:Clonal growth and maturation to immunoglobulin secretion in vitro of every growth-inducible B lymphocyte. 31 12

C3H/HeJ mice do not respond to the polyclonal B-cell activator lipopolysaccharide (LPS) from Escherichia coli; this was first described by Sultzer who observed that mice of this strain did not respond to an intraperitoneal (i.p.) injection of LPS as measured by the accumulation of leukocytes in the peritoneal cavity. Neither were C3H/HeJ mice as susceptible to LPS toxcitiy (1). It was later reported that LPS-induced mitogenesis (2,3), adjuvanticity (4), and the appearance of Ia antigens on B lymphocytes as induced by LPS, (5) was also absent in C3H/HeJ mice. However, lymphocytes from these mice respond normally to the polyclonal B-cell activators purified protein derivative of tuberculin (2,6) and dextran sulfate and have also been reported to respond normally to concanavalin A (Con A) (2). Furthermore, the immune responses to sheep erythrocytes (7) and soluble thymus-dependent antigens (4) are normal in C3H/HeJ mice. Unresponsiveness to LPS in C3H/HeJ mice has been found to Be due to a defect in a single gene or a set of linked genes (3,8) which has been mapped between the major urinary protein locus and the locus coding for polysyndactyly on chromosome 4. (1) We have reported that injection of LPS into mice of an LPS-responsive strain causes a shift in the Con A dose-response curve of cultured spleen cells, suppressing the low does response (9). Therefore, we tested the Con A proliferative response in cultures of normal or LPS-activated spleen cells from LPS-responder (C3H/Tif) and LPS-nonresponder (C3H/HeJ) mice. We report here that C3H/HeJ spleen cells respond poorly to low concentrations of Con A (0.05-0.1 mug/ml). Injection of LPS 2 days before culture inhibits the response to low doses of Con A in cultures of C3H/Tif spleen cells but has no inhibitory effect on the dose response profile of C3H/HeJ spleen cells. Furthermore, the low dose Con A response of spleen cells is dependent upon the presence of an Ia-positive cell. (2) The role of Ia-positive cells in the Con A response of C3H/Tif and C3H/HeJ spleen cells is described.
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PMID:Genetic control of lymphocyte activation: lack of response to low doses of concanavalin A in lipopolysaccharide-nonresponder mice. 33 Jul 92

Rabbit antisera have been prepared against spleen B cells from C3H/Tif mice, high responders to lipopolysaccharide (LPS). After complete absorption on tissues of C3H/Hej mice (LPS nonresponders), such antisera specifically stain and kill (in the presence of complement) a fraction of the B cells from a number of LPS high responder strains, and fail to recognize any cells in two different LPS nonresponder strains, C3H/HeJ and C57B1/10.Sc.Cr. The ontogeny, organ and strain distribution of this B cell marker parallels LPS reactivity. Frequencies of cells stained by this antiserum correspond to the frequencies of LPS-reactive B cell precursors recently determined. This antigent(s) is expressed by LPS-activated B cell blasts but not by cells which remain small after 48 h in the presence of LPS. Removal of the cells recognized by the antisera leads to depletion of LPS-reactive cells, while enriching for reactivity to another B cell mitogen, e.g. lipoprotein.
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PMID:An antiserum which recognizes lipopolysaccharide-reactive B cells in the mouse. 34 58

Three different concentrations of horseradish peroxidase-labelled lipopolysaccharide (LPS-HRP) were added in vitro to spleen cells from the LPS high-responder strain C3H/Tif and to cells from the low-responder strain C3H/HeJ. After being washed and fixed the cells were exposed to the substrate and prepared for electron microscopy. After addition of 7 and 0.7 microgram/ml of labelled LPS only lymphocytes from the high-responder strain were labelled. About 5-10% of the cells from C3H/Tif bound LPS, which is in accordance with the known frequency of B cells possessing the genetically determined LPS receptor. At the highest dose of labelled LPS (70 microgram/ml) a large proportion of lymphocytes from the low-responder strain also bound LPS. Erythrocytes from both strains bound LPS at all concentrations. It is concluded that LPS-HRP allows the detection at the cellular level of LPS binding to the genetically controlled membrane receptor for LPS.
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PMID:Bacterial lipopolysaccharides bind selectively to lymphocytes from lipopolysaccharide high-responder mouse strains. 39 66

The responsiveness of spleen cells from C3H/HeJ and C3H/Tif mice to lipopolysaccharide (LPS) was compared. Around 1,000-fold higher concentration of LPS were required to minimally activate HeJ cells, as compared with Tif high-responder cells, to both proliferation and polyclonal antibody secretion. However, HeJ cells did respond to higher LPS concentrations (100 and 1000 mug/ml). This selective pattern of responsiveness to LPS was also observed in the polyclonal responses of strains to LPS in vivo. Furthermore, the unresponsiveness of HeJ spleen cells was found to depend on a pure B-cell defect in the capacity to interact and/or generate triggering signals on interaction with LPS. Thus, adherent cells, thymus-derived lymphocytes, serum factors, and other non-specific conditions inherent in spleen cell suspensions of low-responder mice were not responsible for suppressing a putative B-cell response to LPS. The present findings are compatible with the possibility that the defect in C3H/HeJ B cells reflects the absence of a structure on the cell surface membrane that is functionally responsible for mediating LPS triggering.
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PMID:Genetic control of B-cell responses. II. Identification of the spleen B-cell defect in C3H/HeJ mice. 108 55

Spleen cells from C3H/Hej mice (H-2k) respond poorly to the B-cell mitogen lipopolysaccharide in vitro as compared to the related strains C3H/Tif (H-2k) and CBA/Orl (H-2k). The electrokinetic properties of splenic lymphocytes from these 3 strains were investigated in parallel, in order to both quantitate low-mobility B cell and high-mobility T cell populations and measure their mean electrophoretic mobilities. C3H/Hej mice were found to possess the same proportion (55%) of LM cells as C3H/Tif and CBA/Orl mice. Therefore, the low LPS-responsiveness of C3H/Hej is not due to a numerical deficiency in B cells. Whereas the mean EPM of HM cells was identical in the 3 strains, that of LM cells was slightly (6%) but significantly (Student's t test, P less than 0.01) lower in C3H/Hej than in the high LPS-responder controls. This suggests that the membrane-structure required for activating interaction with LPS might contribute to B-cell electronegative surface-charge.
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PMID:Electrokinetic properties of splenic lymphocytes from the low-lipopolysaccharide responder C3H/Hej mice. 108 4


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