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

The addition of low doses of the cationic polypeptide antibiotic, polymyxin B (PB), to cultures of mouse spleen cells inhibits lipopolysaccharide-(LPS) induced DNA synthesis but not that stimulated by PPD, PHA, or Con A. Inhibition is stoichiometric; the mitogenic response is suppressed by 50% at a weight ratio of PB:LPS of 0.055 to 1. Furthermore, PB-LPS complexes have a much reduced mitogenic capacity. These complexes inhibit the mitogenic response of spleen cells to unmodified LPS but not to PPD, Con A, or PHA. The inhibitory activity of PB is less effective when added after LPS is mixed with responding cells, achieving 50% inhibition when addition is made at 4 to 6 hr. Time course experiments indicate that partial inhibition is a reflection of a lower rate of DNA synthesis. Thus, PB inhibition of LPS mitogenesis apparently occurs as a result of formation of PB-LPS complexes with reduced mitogenic capacity. Specific inhibition by the complexes of mitogenesis induced by native LPS suggests that the inactive complex may bind to B cells but is unable to trigger them.
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PMID:Inhibition of the mitogenic response to lipopolysaccharide (LPS) in mouse spleen cells by polymyxin B. 18 99

Intraperitoneal treatment of mice with adjuvants affects the in vitro response of their lymphocytes toward class-specific mitogen. Spleen cells from animals injected with Corynebacterium parvum organisms showed in some cases an increase in their response to all mitogens, while in other experiments, a moderate decrease in the reaction to T-specific mitogens (concanavalin A and phytohemagglutinin) was found. Injection of lipopolysaccharide (LPS) and in particular Bordetella pertussis bacteria, brought about a marked reduction in the response of spleen cells to B mitogens (LPS and PPD) but had little or no effect on the reaction to the T mitogens. Intraperitoneal administration of B. pertussis caused a marked depletion of lymph nodes and a high level of lymphocytosis. Blood cells of the treated mice showed an increased response to T mitogens, whereas mesenterial lymph node cultures reacted higher than the controls to LPS and without stimulation. No change was noted in the responses of cells from the axillary lymph nodes of these pertussis-treated mice.
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PMID:Effects of in vivo administered B. pertussis and other adjuvants on the mitotic responses of lymphocytes in vitro. 19 Jan 70

The present studies demonstrate that xenotropic type C virus is efficiently released in response to lipopolysaccharide by spleen cells of a wide variety of inbred mouse strains. Lipopolysaccharide-mediated virus release primarily involves B lymphocytes and is in part genetically determined. Virus release can also be efficiently stimulated by other naturally occurring B cell mitogens, including Nocardia water soluble mitogen, and PPD. The evidence indicates that these agents act synergistically with halogeneated pyrimidines, but not with each other, to cause virus release. These results indicate that B cell mitogens act to release virus by a mechanism that differs from that of halogenated pyrimidines.
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PMID:Genetic factors infuencing mouse type-C RNA virus induction by naturally occurring B cell mitogens. 19 Mar 19

CBA mice recieved a single intraperitoneal injection of hydrocortisone acetate (OHC) in a dose of 125 mg/kg body weight. At various times therafter, electrophoretic mobility (EPM), surface immunoglobulin (SIG) and in vitro DNA synthetic reactivity to concanavalin A (ConA), phytohemagglutinin (PHA), lipopolysaccharide (LPS) and tuberculin (PPD) were investigated on splenic lymphocytes. OHC was found to deplete rapidly the spleen to a minimum of 18% of control cellularity by day 4 posttreatment. At this time, the proportions of low mobility (LM) and SIG-bearing lymphocytes (B cells) were reduced respectively to 28% (control 54%) and 20% (control 45%). The proportion of high mobility (HM) lymphocytes (T cells) was increased to 72% (control 45%). While the mean EPM of LM cells (0.71) was only slightly and transiently reduced, that of HM cells was significantly augmented (1.24) over control value (1.16). This latter finding was interpreted as indicating the selective removal by OHC of a T cell subpopulation with a mean EPM around 1.10. Changes in mitogenic responsiveness were consistent with these alterations of B and T cell compartments. Despite a marked drop in spontaneous 3H-thymidine uptake, the absolute response to T cell mitogens ConA and PHA remained relatively unchanged. By contrast, the reactivity to B cell mitogens LPS and PPD was strongly depressed. Starting by day 12, regeneration and normalizaiton of lymphocyte populations proceeded slowly and were not achieved before day 26-34.
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PMID:Electrokinetic properties and mitogen responsiveness of mouse splenic B and T lymphocytes following hydrocortisone treatment. 30 Jul 13

The purified protein derivative of tuberculin (PPD tuberculin) stimulates approximately one of two lipopolysaccharide (LPS)-activated B-cell blasts of C57BL/6J nu/nu spleen cells to continued clonal growth and maturation to IgM and IgG secretion. It alwo stimulates background, in vivo-activated large cells of normal C57BL/6J nu/nu spleen to growth and Ig secretion, at a frequency of approximately 1 of 100 large spleen cells. PPD tuberculin, therefore, is a polyclonal B-cell activator for B-cell blasts. Many single murine splenic B cells (approximately 50%) appear to have reactivities, and therefore probably receptors, for LPS and PPD tuberculin. PPD tuberculin does not stimulate small, resting B cells to growth as measured by the number of cells in culture and by thymidine uptake. However, it stimulates approximately one-fourth of all spleen cells to blast transformation. The large-size blast cells secrete IgM and, therefore, form plaques in the protein A plaque assay. IgG-secreting, plaque-forming cells develop at later stages of stimulation, indicating that the switch from IgM to IgG may occur without division in single, stimulated B cells. Stimulation of resting B cells to maturation by PPD tuberculin is polyclonal. Thus, approximately 1 in 10(2) IgM-secreting plaque-forming cells form plaques with trinitrophenyl-substituted sheep erythrocytes, 1 in 450 do so with horse erythrocytes, and 1 in 10(3) with sheep erythrocytes. Furthermore, the number of Ig-secreting cells developing from small, resting cells without growth in cultures with or without filler thymus cells suggests polyclonal activation by PPD tuberculin to maturation only of at least one out of four small, splenic B cells.
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PMID:The purified protein derivative of turberculin, a B-cell mitogen that distinguishes in its action resting, small B cells from activated B-cell blasts. 31 90

The effect of treatment with the methanol extraction residue (MER) mycobacterial fraction on the immunological responsiveness of BALB/c mice to the T-independent antigens pneumococcal polysaccharide type III (SIIII) and trinitrophenyl-lipopolysaccharide conjugate (TNP-LPS) was ascertained. Pretreatment with MER prevented the establishment of immunological paralysis by threshold doses (10 or 15 microgram) of SIII and by a paralyzing dose of 100 microgram TNP-LPS. The induction of immunological paralysis by SIII was unaffected by treatment with the bacterial adjuvant Corynebacterium parvum and with the B cell mitogens PPD, LPS (Escherichia coli lipopolysaccharide), and dextran sulfate.
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PMID:Effect of the MER tubercle bacillus fraction on the responsiveness of mice to T-independent antigens. 37 26

Endotoxin protein, an outer membrane protein of Gram-negative bacteria associated with lipopolysaccharide endotoxin, has been found to be a potent activator of lymphocytes. In the absence of T lymphocytes and macrophages, endotoxin protein can stimulate murine B lymphocytes to synthesize DNA and produce antibodies of diverse specificities. This stimulation is greater than that obtained with two well known murine B cell activators, lipopolysaccharide endotoxin or PPD-tuberculin. Splenic lymphocytes from other species, such as rats, rabbits, and guinea pigs also proliferate when cultured with endotoxin protein. Of particular significance is the finding that endotoxin protein is an activator of human peripheral blood lymphocytes.
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PMID:Further studies on the activation of lymphocytes by endotoxin protein. 37 15

Soluble mediators, lymphokines, released by stimulated lymphoid cells can modify immunological responses in several ways. In this investigation we have examined whether the supernatants of phytohaemagglutinin (PHA)-activated human lymphocytes (active SUPs) contain factors that can suppress proliferative responses of lymphocytes in vitro. The results have shown that crude preparations of peripheral lymphoid cells incubated for 24 h in active SUPs can suppress the responses of cocultured autologous lymphocytes to PPD tuberculin in vitro. Their suppressive activity was not abolished by mitomycin treatment. Some reduction of phytomitogen responses was also noted. Maximal suppressive activity was obtained within 24 h of incubation in active SUPs and it could not be induced in cell preparations depleted of monocytes-macrophages. Similar results were obtained by treating lymphoid cells with lipopolysaccharide from Escherichia coli, which is a known activator of monocytes. These results thus show that lymphokines released by stimulated lymphoid cells can activate monocytes-macrophages in such a way that they become immunosuppressive.
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PMID:Evidence that soluble products released by PHA-stimulated human lymphoid cells activate immunosuppressive monocytes. 41 64

A group of thirty-five mothers and their babies at parturition were examined by the in vitro lymphocyte transformation test to determine sensitization by oral bacterial antigens, B-cell mitogens and dental plaque. Lymphocytes from babies of sensitized mothers with gingival or periodontal disease gave the highest frequency (70 and 63%) and magnitude (mean stimulation index of 3.4 and 3.3) of response in cultures stimulated by Actinomyces viscosus and Veillonella alcalescens. However, IgM antibodies to V. alcalescens antigen were absent from cord sera. With one exception, stimulation of lymphocytes from babies of unsensitized mothers with clinically healthy gingiva was not found with these antigens. The response of cord lymphocytes from mothers with gingival or periodontal disease to antigens from oral bacteria, as compared with the response of cord lymphocytes from mothers with clinically healthy gingiva, seemed specific, since a corresponding difference in response to unrelated antigen PPD was not found. The response of cord and maternal lymphocytes to B-cell mitogens was also determined. Maternal lymphocytes responded in the following decreasing order of effectiveness: dextran sulphate, levan, lipopolysaccharide and dextran B1355; whereas cord lymphocytes were stimulated in the reverse order of effectiveness.
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PMID:Interdependence of in vitro responsiveness of cord and maternal blood lymphocytes to antigens from oral bacteria. 60 45

Two derivatives of wax D, one possessing immunogenicity and the other adjuvant activity, were tested for the possible role in the induction of adjuvant arthritis (AA) in rats. The former, a water-soluble arthritogenic and immunogenic component (WAC), in incomplete Freund's adjuvant, was able to induce delayed hypersensitivity (DH) and mild AA, but failed to function as an adjuvant in rats. The latter, an acetylated wax D (AD) and its subfraction, AD6, did exert adjuvant activity, but were free from immunogenicity and arthritogenicity. The addition of AD or AD6 to the WAC in incomplete Freund's adjuvant, when injected into inguinal lymph nodes, resulted in the production of severe AA with high incidence. Other adjuvants such as pertussis vaccine and lipopolysaccharide could not replace AD6; they failed to enhance AA when combined with the WAC. Also, other mycobacterial antigen, PPD, could not replace wax D-derived WAC; it did not induce AA when coupled with AD6, although it did induce DH to PPD.
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PMID:Synergism of immunogenic and adjuvant-active components of mycobacterial wax D in the induction of adjuvant arthritis. 82 21


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