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

In recent years, murine and human virgin B lymphocytes have been used to examine the steps necessary for polyclonal activation. In these models mitogens are used in conjunction with lymphokines to determine which signals are responsible for regulating B-cell triggering, proliferation, and differentiation. While progress has been made in understanding these events as they occur in virgin B cells, very little evidence exists to suggest whether these models of activation also apply to the memory B-cell population. In this report we have described an antigen-specific, secondary in vitro immune response using cells isolated from lymph nodes draining the site of antigen injection. Unfractionated cells, B cells, and size-fractionated cells from dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH)-primed rats were challenged in vitro with DNP-KLH, lipopolysaccharide plus dextran sulfate (LPS/DxS), and T-cell factors. We have consistently found, under all these conditions, that antigen challenge of primed cells results in the production of DNP-specific IgG antibody while stimulation with LPS/DxS plus T-cell factors results only in the polyclonal activation of virgin B cells; no antigen-specific IgG secretion is seen. This suggests that acquisition of memory status is associated with a loss in responsiveness to LPS/DxS-induced differentiation.
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PMID:Polyclonal activation of primed rat B cells. 242 21

Several studies have indicated that thymus-independent (TI) antigens, unlike their thymus-dependent (TD) counterparts, are poor at generating memory antibody responses (Immunol. Today 1981. 3:217). In contrast to this view, the present report shows that the TI type 1 (TI-1) antigen, 2,4,6-trinitrophenyl-lipopolysaccharide (TNP-LPS), elicits good secondary responses in rats. These secondary antibody responses are not only greater in magnitude than the primary responses, but display a different pattern of Ig classes with more IgG and IgA antibodies produced. In transfer experiments between congenic strains of rats which differ in their kappa light chain Ig allotype, it is shown that this memory is attributable to persistent B cell clones. The TI-2 antigen, 2,4-dinitrophenyl-hydroxyethyl starch (DNP-HES), given alone did not elicit B cell memory. However, when DNP-HES is presented to the immune system in association with LPS, the pattern of the anti-DNP response is similar to that elicited by TNP-LPS. The capacity to generate TI memory is associated with the appearance of hapten-specific B cells in the marginal zones of the spleen. Hapten-binding cells were induced in the marginal zones following immunization with TNP-LPS, but not by DNP-HES. However, concurrent immunization with DNP-HES and LPS which were not covalently linked was found to induce DNP-binding cells in the marginal zone. There is complete correlation between the appearance of hapten-binding memory B cells in the marginal zone and the capacity of these antigens to induce secondary responses.
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PMID:B cell memory to thymus-independent antigens type 1 and type 2: the role of lipopolysaccharide in B memory induction. 245 43

The murine antibody response to T-independent (TI)-2 antigens [2,4-dinitrophenyl-Lys-Ficoll (DNP-FIC) and DNP-hydroxyethyl starch (HES)] was impaired long after splenectomy, while responses to TI-1 [trinitrophenylated lipopolysaccharide (TNP-LPS)] and thymus-dependent [TNP-keyhole limpet hemocyanin (KLH)] antigens were largely unaffected. The antibody response to these TI-2 antigens was exclusively against the conjugated epitopes [DNP-, fluorescein isothiocyanate (FITC)- or tetramethylrhodamine isothiocyanate (TRITC)-Ficoll or -HES]. Fluorescent conjugates of Ficoll and HES localize selectively to the splenic marginal zone macrophages. This localization was not affected by 750 cGy of X-irradiation, but the antibody response to the TI-2 antigens was abrogated for 14 days. Administration of spleen cells restored the antibody response to these TI-2 antigens in otherwise intact irradiated mice but not if they had been splenectomized. Our findings indicate that the antibody response to TI-2 antigens depends upon stimulation of B cells in a splenic environment. This probably involves antigen presentation by marginal zone macrophages.
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PMID:Splenic dependence of the antibody response to thymus-independent (TI-2) antigens. 258 91

The immunosuppressive effects of 2-acetylaminofluorene (AAF) and 2-aminofluorene (AF) were studied in BALB/c mouse splenocyte culture. Direct addition of AAF and AF to the splenocyte culture produced a dose-related suppression of the in vitro antibody response to sheep erythrocytes(SRBC), DNP-Ficoll, and lipopolysaccharide(LPS). AAF and AF also produced suppression on lymphoproliferative responses to LPS and concanavalin A(Con A). The immunosuppressive effects of AAF and AF, however, were diminished when AAF and AF were incubated in the splenocyte-hepatocyte coculture system for 4 hr. When hepatocyte cultures were pretreated with SKF 525A, a cytochrome P-450 inhibitor, before coculture with spleen cell along with AAF and AF, the suppression of in vitro antibody response reappeared. Meanwhile, both AAF and AF produced a dose-related DNA single-strand breaks in spleen cells only if AAF and AF were treated to spleen cells cocultured with hepatocytes. These results indicate that the immunosuppression by AAF and AF is not mediated by the reactive metabolites implicated to DNA damage.
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PMID:Immunosuppressive effects of 2-acetylaminofluorene and 2-aminofluorene on murine splenocytes culture. 263 48

The effects of carbon tetrachloride (CCl4), following 7 consecutive days of exposure ip at 500, 1000, and 1500 mg/kg, were determined on murine humoral and cell-mediated immune responses, body and organ weights, spleen cell blastogenesis following mitogenic stimulation, and clinical serum parameters for liver injury. In vivo sensitization of CCl4-treated B6C3F1 mice resulted in a dose-dependent suppression of the T-dependent antibody response to sheep red blood cells (sRBC) at all doses--36, 48, and 53%, respectively. The T-independent in vivo antibody response to DNP-Ficoll was suppressed only at 1500 mg/kg, and only by approximately 16%. This dosing regimen also resulted in a significant decrease in thymus weights; however, there were no significant effects on liver, kidney, lung, or body weights. The serum chemistry profile indicated a dose-dependent increase in serum glutamic-pyruvic transaminase (SGPT) levels (34-, 47-, and 55-fold) and a non-dose-dependent increase in serum bilirubin and total protein. Serum glucose and albumin levels were unaffected. Splenocytes from mice treated with 1500 mg/kg and sensitized in vitro with antigen demonstrated a comparably suppressed antibody response to the antigens sRBC and DNP-Ficoll as observed in vivo--66 and 28% respectively. This dose of CCl4 had no effect on the in vitro antibody response to the polyclonal antigen lipopolysaccharide. The mixed lymphocyte response was dose dependently suppressed following CCl4 exposure; however, the delayed-type hypersensitivity response was unaffected. Lymphocyte blastogenesis following mitogenic stimulation with lipopolysaccharide or concanavalin A was also inhibited by CCl4 exposure. These studies demonstrate that exposure to CCl4 results in a marked suppression in both humoral and cell-mediated immune responses at concentrations which also affect the liver as evidenced by the marked increase in SGPT levels.
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PMID:Suppression of humoral and cell-mediated immune responses by carbon tetrachloride. 292 10

The present study was undertaken to compare the effects of two adjuvants, SGP (a starch-acrylamide polymer) and Quil A (purified saponin), with that of aluminum hydroxide (Al(OH)3) on murine primary antibody responses to T-independent (TI) and T-dependent (TD) antigens. All three adjuvants augmented the responses to the TD antigens, dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH), and sheep erythrocytes (SRBC). SGP was the most potent adjuvant and increased the primary IgG response to DNP-KLH as much as 90-fold. Quil A and Al(OH)3 had comparable effects on the primary response to DNP-KLH, but Quil A was less effective than Al(OH)3 for augmenting the primary response to SRBC. Quil A and SGP both augmented the primary IgM and IgG responses to trinitrophenyl-lipopolysaccharide (TNP-LPS), TNP-Brucella (TI-1 antigens), and TNP-Ficoll (TI-2 antigens). Al(OH)3, like most commonly used adjuvants, had little or no effect on responses to TI antigens. The kinetics of the response to TNP-Ficoll was altered by SGP, since peak responses were maintained for at least 7 days, while the response to TNP-Ficoll alone peaked on Day 4 and had declined considerably by Day 7. Both SGP and Quil A could augment responses to both optimal and suboptimal doses of antigen. The adjuvant activity of SGP was diminished, but still effective, when smaller amounts of SGP were used with the immunizing antigen, and all three adjuvants were able to augment primary responses when given in separate injections from the antigen. These results demonstrate that SGP is a very effective adjuvant, and show that both Quil A and SGP have a unique ability to increase antibody responses to TI antigens, suggesting that their effects may be mediated at least partially through B cells.
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PMID:Immunopotentiating effects of the adjuvants SGP and Quil A. I. Antibody responses to T-dependent and T-independent antigens. 348 57

The adjuvants SGP (a starch-acrylamide polymer) and Quil A (purified saponin) were shown to markedly augment antibody responses to T-independent (TI) antigens, suggesting that their adjuvant effects may be at least partially mediated through B cells. The ability of both adjuvants to augment primary responses to trinitrophenyl (TNP)-Ficoll (TI-2 antigen) in athymic nude mice further suggested these adjuvants affect B cells. SGP, however, did not induce a response to the T-dependent (TD) antigen dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH) in athymic nude mice, indicating it was unable to replace the requirement for T-helper cells for responses to TD antigens. Responses to TNP-lipopolysaccharide (LPS) were augmented by SGP in CBA/N X Balb/c immune defective (xid) mice. However, SGP was unable to induce a response to TNP-Ficoll in xid mice. The SGP and Quil A augmented responses to TNP-Ficoll were completely inhibited by the mitotic inhibitor, Velban, indicating that SGP and Quil A increased the plaque-forming cell (PFC) response primarily by stimulating cell proliferation, and not by recruitment of antigen-reactive cells. The effects of the adjuvants on secondary responses were investigated using adoptive transfer experiments. SGP and A1(OH)3 both increased the induction of hapten-specific memory B cells in mice primed with DNP-KLH. SGP, Quil A, and A1(OH)3 also increased priming of carrier specific T cells. Priming of memory B cells with DNP-KLH and either A1(OH)3 or SGP was prevented when T cells were depleted with anti-lymphocyte serum (ALS) at the time of antigen priming, indicating that the augmentation of memory B-cell priming by SGP and A1(OH)3 was dependent on the presence of functional T cells. SGP and Quil A were both unable to augment memory cell induction to the TI antigen, TNP-Ficoll, even though both adjuvants markedly augmented primary IgM and IgG responses to this antigen. Based on these results, it is suggested that SGP and Quil A can mediate their adjuvant effects primarily by a direct or indirect effect on B cells although the adjuvants may also affect T cells to some extent.
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PMID:Immunopotentiation by SGP and Quil A. II. Identification of responding cell populations. 348 58

The immunomodulating effect of lobenzarit disodium (CCA, disodium 4-chloro-2,2'-iminodibenzoate), was examined in restraint-stressed mice which exhibited immunodeficient conditions mainly based on dysfunction of helper T cells. Primary direct plaque-forming cell (PFC) responses to T cell-dependent antigens such as sheep red blood cell (SRBC) and dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH) were severely diminished by restraint-stress, whereas responses to T cell-independent antigens such as DNP-Ficoll (DNP-Fic) and trinitrophenyl-lipopolysaccharide (TNP-LPS) were little reduced and sometimes were even increased. CCA, orally administered to mice at a dose of 50 mg/kg body weight, significantly restored anti-SRBC PFC response. Restraint-stress also markedly decreased the proliferative response of splenic lymphocytes to concanavalin A (Con A), while it slightly augmented the response to lipopolysaccharide (LPS). CCA increased the response to Con A and suppressed the response to LPS. The number of T and B lymphocytes in the spleen were, however, reduced to the same degree by the stress and there was no striking difference in the susceptibility of these two subpopulations of splenic lymphocytes as analysed with fluorescein-activated cell sorter. CCA increased both T and B lymphocytes, but Lyt-1+ (helper/inducer T) cells recovered even more. It is noteworthy that in all these experiments CCA restored the weight of the thymus which is considered to be one of the organs most sensitive to stress. These results indicate that CCA promotes proliferation and differentiation of T cells, especially helper T cells, and restores immune functions depressed by restraint-stress.
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PMID:Alleviation of depressed immunity caused by restraint-stress, by the immunomodulator, lobenzarit disodium (disodium 4-chloro-2,2'-iminodibenzoate). 362 69

Humoral immunity of casein-treated B6C3F1 mice was evaluated. Splenocytes from casein-treated mice sensitized in vitro exhibited a marked suppression in their antibody response to the T-dependent antigen, SRBC (82%) and T-independent antigen, DNP-Ficoll (80%). In contrast, a control response to the polyclonal antigen, lipopolysaccharide (LPS), was observed. Cell fractionation and crossover reconstitution assays of adherent (ADH) and nonadherent (NAD) splenocyte populations from vehicle and casein-treated mice indicated that: 1) ADH splenocytes from casein-treated mice were responsible for suppression of humoral responses, 2) NAD splenocytes from casein-treated mice reconstituted with vehicle or naive ADH cells abrogated the immunosuppression, and 3) suppression of humoral responses in cultures containing casein ADH splenocytes was due to this cell populations inability to function as accessory cells in humoral responses rather than induction of suppressor macrophages. Results from in vivo studies with casein-treated mice sensitized with sheep red blood cells or dinitrophenyl-Ficoll paralleled the in vitro results.
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PMID:Inhibition of macrophage accessory cell function in casein-treated B6C3F1 mice. 362 70

Repair of injury induced by freeze-drying Salmonella anatum in nonfat milk solids occurred rapidly after rehydration. Injury in surviving cells was defined as the inability to form colonies on a plating medium containing deoxycholate. Death was defined as inability to form colonies in the same medium without this selective agent. The rate of repair of injury was reduced by lowering the temperature from 35 C to 10 C and was extremely low at 1 C. Repair was independent of influence of pH between 6.0 and 7.0. Repair did not require synthesis of protein, ribonucleic acid, or cell wall mucopeptide, but did require energy in the form of adenosine triphosphate (ATP) synthesized through oxidative phosphorylation. The requirement for ATP was based on dinitrophenol or cyanide interference with repair. Dinitrophenol activity was pH-dependent; no repair occurred at pH 6.0 and some repair was observed at pH 6.5 and above. Injured cells were extremely sensitive to low concentrations of ethylenedinitrilotetraacetate. This indicated that freeze-drying injury of S. anatum may involve the lipopolysaccharide portion of the cell wall and that repair of this damage requires ATP synthesis.
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PMID:Repair of injury in freeze-dried Salmonella anatum. 500 Aug 67


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