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)

Daily gastric intubation of lipopolysaccharide (LPS)-responsive C3H/HeN, BALB/c, and Swiss mice with SRBC for 2 wk resulted in oral tolerance, whereas similarly treated LPS-nonresponsive C3H/HeJ mice gave splenic anti-SRBC PFC responses, including the IgA isotype, after systemic challenge with antigen. Oral tolerance in LPS-responsive C3H/HeN mice was due to T suppressor (Ts) cells because significant Ts cell activity was demonstrated in both Peyer's patches (PP) and spleens of these animals. On the other hand, T cells from PP and spleens of identically treated C3H/HeJ mice exhibited mainly T helper cell activity. Prior treatment of PP or spleen cell preparations from tolerant C3H/HeN mice with anti-Lyt-2.1 resulted in good in vitro anti-SRBC PFC responses, especially IgA isotype responses in PP cell cultures. These results indicate that oral administration of a thymic-dependent antigen (SRBC) to LPS-responsive mice induced a Ts cell population in PP, which, after migration to peripheral lymphoid tissue (e.g., spleen), suppressed responses to systemically administered antigen. LPS-nonresponsive mice lack this Ts cell pathway and continually respond to oral administration of antigen.
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PMID:Lack of oral tolerance in C3H/HeJ mice. 703

Aminocarb, a phenylsubstituted methylcarbamate pesticide (4-dimethylamino-3-methyl-N-carbamate; matacil), previously suspected of a relatively low immunotoxic potential, was administered by four different exposure routes to C57BL/6 mice. A single sublethal exposure by oral and dermal routes stimulated humoral immune response at a relatively low dose; 1/256 LD50 of aminocarb. Intraperitoneal (i.p.) injection decreased the humoral PFC response, whereas inhalation of aminocarb had no marked effect on peripheral immune status in exposed animals. Thus, i.p. exposure resulted in higher immunotoxicity over oral administration of aminocarb. Similarly, marked route-related exposure differences in immunomodulatory effects of aminocarb were noted for mitogenic stimulation of spleen lymphocytes and mixed lymphocyte response. Other indices, such as delayed type hypersensitivity (DTH) and production of interleukin-2 (IL-2) were unchanged. Interestingly, expression of major histocompatibility complex (MHC) class II by purified, lipopolysaccharide (LPS)-stimulated B cells increased equally after i.p. and oral exposures to aminocarb. Overall, a weak immunosuppressive potential of aminocarb was concluded, which was possibly due to indirect interaction of the pesticide with the immune system. However, aminocarb may represent an autoimmunity-inducing toxic.
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PMID:Immunotoxicity of aminocarb. III. Exposure route-dependent immunomodulation by aminocarb in mice. 776 98

An enzyme-linked immunosorbent assay (ELISA) was developed to detect IgM and IgG antibodies specific for trinitrophenyl-lipopolysaccharide (TNP-LPS). Treatment of C57BL/6 and DBA/2 mice with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other aryl hydrocarbon (Ah) receptor agonists followed by immunization with TNP-LPS resulted in a dose-dependent decrease in serum IgM which paralleled the decrease in the splenic PFC response. The ED50 values for the IgM and splenic PFCs in C57BL/6 mice for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3,3',4,4',5-pentachlorobiphenyl (pentaCB) and 3,3',4,4',5,5'-hexaCB were 2.8 and 1.6, 11 and 14, and 25 and 20 micrograms/kg, respectively; in the less Ah-responsive DBA/2 mice, the ED50 values were 8.5 and 10, 61 and 69, and 73 and 71 micrograms/kg, respectively. In addition, treatment of C57BL/6 mice with TCDD resulted in alterations of serum IgG relative to IgM and a delay of isotype switching was observed after immunization and boosting with TNP-LPS. This ELISA may prove to be a useful tool in monitoring immune function during long-term exposure of mice to TCDD and related compounds and exploring the mechanism of Ah receptor-mediated immunosuppression.
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PMID:An enzyme-linked immunosorbent assay (ELISA) specific for antibodies to TNP-LPS detects alterations in serum immunoglobulins and isotype switching in C57BL/6 and DBA/2 mice exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds. 794 May 57

In these studies, the food promutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) was evaluated for its immunotoxicity in B6C3F1 mice following oral 5-day dosing at total doses of 50 and 150 mg/kg. Results indicated that PhIP produced a dose-dependent suppression of the humoral immune response of spleen cells to sheep erythrocytes, with a 50% decrease in the number of PFC detected at the 150 mg/kg dose of PhIP. A 40-90% inhibition of the phytohemagglutinin (PHA) response of spleen cells, mesenteric lymph nodes (MLNs), and Peyer's patch (PP) lymphocytes was seen in the treatment groups. The lipopolysaccharide (LPS) response was somewhat more variable and less affected with 20-30% inhibition observed in the spleen and PPs, whereas PhIP increased the LPS response in the MLNs. There was no effect of PhIP on cell recovery or viability in any of the treatment groups. Flow cytometry analysis revealed a depletion of T cells (Thy 1.2+ cells) and a slight increase in B cells (Ly5+ cells) in the PPs. The percentage of B and T cells present in the spleen and MLNs was unaffected by PhIP. These results demonstrate that the oral administration of PhIP produces immunotoxicity to mice, especially to lymphoid tissues present in the GI tract (i.e., PPs), and demonstrates that T cell mitogen (PHA) responses in PPs are the most sensitive indicator of PhIP-induced immunotoxicity.
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PMID:Inhibition of humoral immunity and mitogen responsiveness of lymphoid cells following oral administration of the heterocyclic food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) to B6C3F1 mice. 795 67

Properdin is the only known positive regulator of the alternative pathway of complement activation. Northern blot analysis of cell lines derived from fibroblasts, B-cells, hepatoma cells, and cells of the monocyte-macrophage lineage revealed properdin expression only in the myelomonocytic cell line HL-60, in the monoblastic cell line U-937 and in the monocytic line Mono Mac 6. Culture of Mono Mac 6 cells for 24 h with phorbol 12-myristate 13-acetate, bacterial lipopolysaccharide and the cytokines interleukin-1 beta and tumour necrosis factor-alpha enhanced mRNA abundance, with the strongest effect (tenfold) being observed with the lipopolysaccharide. In contrast, recombinant interferon-gamma consistently halved properdin mRNA abundance. The same pattern was found for the secretion of properdin as detected by ELISA of Mono Mac 6 supernatants. The suppressive effect of interferon-gamma on properdin mRNA abundance was also demonstrated for primary blood monocytes. The data suggest that the expression and secretion of this complement regulatory protein by monocytes is differentially regulated by cytokines and link the immune response with alternative pathway activation.
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PMID:Expression of properdin in human monocytes. 811 26

A procedure using enzyme-linked immunosorbent assays for the assessment of complement function has been evaluated. The sera investigated were incubated in microtiter plates with solid-phase complement activators. Human polyclonal IgG or monoclonal IgM were used for classical activation pathway assays and Salmonella typhosa lipopolysaccharide (LPS) for alternative activation pathway assays. The analysis focussed on deposition of C9 and properdin as detected with enzyme-conjugated antibodies. In an attempt to avoid spurious results due to rheumatoid factors in patient sera, monoclonal mouse and chicken antibodies were unsuccessfully tested as indicator reagents in the assay with solid-phase IgG. However, the use of solid-phase IgM as an activator completely circumvented the influence of rheumatoid factors. With solid-phase IgG or IgM, properdin deposition occurred in the absence of factor D. A combination of assays is suggested for diagnostic purposes: IgM-coated plates with detection of bound C9 and properdin for the classical pathway and LPS-coated plates with detection of bound properdin for the alternative pathway. The procedure distinguished between defects of the classical activation pathway (C1, C4, C2), the alternative activation pathway (C3, factor B, factor D, properdin) and the terminal components (C5-C9). This analytical approach may be useful for detection of inherited complement deficiency and the assessment of complement function in acquired complement deficiency states.
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PMID:New procedure for the detection of complement deficiency by ELISA. Analysis of activation pathways and circumvention of rheumatoid factor influence. 828 79

In order to induce an optimal plaque-forming cell response to sheep red blood cells (anti-SRBC PFC response) in vitro, murine splenocytes have been cultured in RPMI 1640 medium containing 10% fetal calf serum (FCS). In this paper, we report that 10% intact FCS in such a conventional medium can be replaced by 2% modified FCS which has been exposed to insoluble polymer beta-cyclodextrin (CD). The most efficient procedure of treatment of FCS was an incubation of 1/50 diluted FCS with 20 mg/ml polymer beta-CD for 3.5 h at 20 degrees C. The PFC response supported by 2% polymer beta-CD-treated FCS, was the same as that obtained when mixing 10% FCS, and was completely dependent on the existence of antigen (SRBC) and enhanced by 2-mercaptoethanol. The time-course profiles of the PFC responses induced in both cultures were almost the same. The 2% polymer beta-CD-treated FCS-containing medium was also effective in inducing both a primary PFC response to the T cell-independent antigen (trinitrophenyl-lipopolysaccharide) and a polyclonal PFC response stimulated by lipopolysaccharide. Inactive FCS lots (so called deficient lots) also became fully supportive at 2% after treatment with polymer beta-CD. These results indicate that polymer beta-CD-treated FCS is not economical for supporting antibody production, but also useful for those experiments on isolation and analysis of factors derived from cultured lymphocytes.
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PMID:Application of polymer beta-cyclodextrin-treated fetal calf serum to in vitro antibody production. 844 48

This study was designed to test the hypothesis that nitric oxide (NO) mediates the blunted splenic sympathetic response to lipopolysaccharide (endotoxin) that occurs in young rats exposed to alcohol in utero (FAE). The subjects, 26-29-day-old rats, were progeny of pregnant dams fed an alcohol diet (35% of the calories were derived from ethanol) or their control and pair-fed (PFC) cohorts. We examined the effects of lipopolysaccharide (LPS) (0.5 mg/kg, i.p.) on splenic norepinephrine (NE) turnover, an index of sympathetic neural activity, splenic inducible NO synthase (iNOS) protein immunoreactivity, and NO metabolites nitrite/nitrate concentrations in plasma. In response to LPS, splenic NE turnover was increased by more than twofold in the PFC groups, but the increase did not occur in their FAE cohorts. The blockade of NOS with L-NAME (30 mg/kg, i.p.) reversed this difference. In both the PFC and FAE rats, basal levels of splenic iNOS protein immunoreactivity were equally barely detected and plasma NO metabolite levels were relatively low (25 microM in both groups). In response to LPS, however, iNOS protein displayed a marked increase in the PFC group and an even greater increase (by close to threefold) in the FAE rats. LPS also substantially increased plasma NO metabolite levels by close to eightfold in the control groups, but by 15-fold in their FAE cohorts compared to the basal levels. These findings support the hypothesis that in the FAE rat, an augmented NO formation accounts for the blunted sympathetic response to endotoxin.
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PMID:Splenic sympathetic response to endotoxin is blunted in the fetal alcohol-exposed rat: role of nitric oxide. 965 Jun 32

The functional status of the immune system of female mice exposed to a single oral dose of dimethoate (16 mg/kg) was evaluated by assessing cell mediated and humoral immune responses, in addition to the effect of dimethoate on spleen and body weights after different time intervals. The data showed that dimethoate caused a time-depended decrease in spleen weights in the absence of a change in body weights. The immunologic effect of dimethoate to female mice produced a dose-dependent decrease in the number of the rosette forming cells (total and active erythrocyte rosette). The ability of splenocytes to proliferation in response to mitogens; phytohemagglutinin (PHA) for T cell and lipopolysaccharide (LPS) for B cell were significantly decreased at the different times. As compared to control, a significant decrease in serum total immunoglobulins (Ig) and IgM was found, while IgG was non-significant deceased. Results of this study also revealed that dimethoate caused a significant decrease in the number of plaque forming cell (PFC/10(6) splenocytes) in a time dependent manner.
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PMID:Effect of dimethoate on the immune system of female mice. 1069 56

The administration of a single small dose of bacterial lipopolysaccharide produces in mice a considerable rise in properdin levels. This is accompanied by an early, transient, non-specific increase in resistance to certain bacterial infections. Bacterial lipopolysaccharides were shown to possess far greater activity than other substances previously studied in bringing about an elevation of properdin levels. After the injection of bacterial lipopolysaccharides, high molecular weight substances appear in the circulation, which interfere with the combination of properdin with zymosan and thus affect the assay of properdin. The administration of small amounts of bacterial lipopolysaccharides to mice at appropriate times before experimental infection "conditions" the mice so that they maintain normal or elevated properdin titers during the infectious process in contrast to control mice which show a progressive decline in properdin to low levels and death. The significance of this observation and its relationship to natural resistance to Gram-negative pathogens are considered.
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PMID:Elevation of properdin levels in mice following administration of bacterial lipopolysaccharides. 1331 94


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