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)

Tumor necrosis factor-alpha (TNF-alpha), which is produced mainly by monocyte/macrophage cells, has diverse physiological functions on lymphoid cells. Moreover, it has been shown that TNF-alpha exhibits antiviral activities. Here we report that Epstein-Barr virus (EBV), a B lymphotropic human herpes virus that interacts intimately with the immune system, exerts a strong inhibitory effect on TNF-alpha production by lipopolysaccharide-treated peripheral blood leukocytes as well as by monocytic cell lines, HL-60 and U-937. Flow cytometric analysis following staining with OKB7 monoclonal antibody showed that about 20% of cells from these monocytic lines express the CR2 antigen. Direct binding of fluorescein isothiocyanate-labeled EBV indicated that the virus binds to approximately 22% of cells of both monocytic lines. However, no virus-specific antigens were detected in the infected cells by immunofluorescence, suggesting that the infection was of the abortive type. The use of UV- or heat-inactivated EBV and inhibitory effect on TNF-alpha synthesis. These results suggest that infectious virus is necessary to obtain such an inhibitory effect. Analysis of TNF-alpha mRNA by polymerase chain reaction amplification indicated that the EBV suppressive effect is manifested at the transcriptional level. In contrast, EBV did not inhibit interleukin 1 mRNA production by these cells. These results indicate that EBV interacts directly with monocytes/macrophages to exert its immunomodulatory effect.
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PMID:Inhibition of tumor necrosis factor-alpha transcription by Epstein-Barr virus. 184 16

Actinobacillus pleuropneumoniae produces several hemolysins/cytotoxins that may be important in the pathogenesis of acute lesions. Little is known, however, about the role of these virulence factors in chronic disease or the carrier state. We investigated the effects of live bacterial infection and transthoracic injection of a sterile culture supernatant on primary lymphoid organs and lymphocyte populations. Transthoracic inoculation of mice or intranasal inoculation of pigs with virulent A. pleuropneumoniae serotypes 1 and 7 induced thymic cortical lymphoid necrosis. These lesions were reproduced in mice by transthoracic injection of a concentrated sterile culture supernatant. The cytotoxic effect of this culture supernatant was also demonstrated in vitro by using a tetrazolium dye reduction assay. Both porcine and murine thymic lymphocytes as well as splenic T lymphocytes were susceptible to the toxin. Porcine convalescent serum, but not preimmune serum, prevented thymic lesions and neutralized the in vitro cytotoxic effect of the culture supernatant on murine thymic lymphocytes. Thymic lesions also were reproduced in mice by using purified lipopolysaccharide (LPS) from Escherichia coli O111:B4; however, LPS had no in vitro cytotoxic effect on either porcine or murine thymic lymphocytes. These results suggest that secreted A. pleuropneumoniae toxin(s) is capable of affecting host T-lymphocyte populations and may affect host immune function.
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PMID:Actinobacillus pleuropneumoniae-induced thymic lesions in mice and pigs. 187 15

In silicosis, alveolar macrophages (AM) are thought to induce chronic inflammation and fibrosis by release of cytokines. Rats were exposed to aerosols of alpha-quartz and examined 4 to 9 mo later for persistence of silica particles and release of tumor necrosis factor-alpha (TNF-alpha) from macrophages. Silica particles were detected in AM, lung parenchyma, and thoracic lymphoid organs, whereas extrathoracic lymphoid tissues and organs were free of the mineral. When AM were tested functionally, no spontaneous release of TNF-alpha was observed. However, upon in vitro stimulation of AM from silicotic rats with a low concentration of lipopolysaccharide (10 ng/ml), abundant TNF-alpha production was found that was higher and occurred more rapidly than with AM from sham-exposed animals. Peritoneal macrophages, which did not have contact with silica particles, displayed a similarly enhanced TNF-alpha release in response to low doses of lipopolysaccharide. These data demonstrate a state of systemic preactivation ("priming") of macrophages that supports the notion that silicosis is associated with a general immunostimulation.
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PMID:Systemic macrophage stimulation in rats with silicosis: enhanced release of tumor necrosis factor-alpha from alveolar and peritoneal macrophages. 191 Aug 24

In order to study the role of nasal-associated lymphoid tissue (NALT) in the local nasal immune response, rats were immunized intra-nasally with either of the following trinitrophenylated (TNP) antigens; the thymus-dependent keyhole limpet haemocyanin (KLH), or the thymus-independent lipopolysaccharide (LPS), or with the particulate (thymus-dependent) sheep red blood cells (SRBC). Primary responses hardly occurred, while only TNP-KLH elicited a considerable secondary response. The major responding organ was the posterior cervical lymph node. Specific antibody-forming cells (AFC) occurred in the medulla and were mainly of the IgA or IgG isotype. Hardly any specific AFC were found in NALT or the surrounding mucosa. Intranasal immunization evoked no antibody response in the lung. Ample anti-TNP antibodies could be detected in the sera of animals, primed and boosted with TNP-KLH or TNP-LPS. No specific serum antibodies occurred after immunization with TNP-SRBC. The results are discussed in view of the immunological defence in the upper respiratory tract.
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PMID:Mucosal and systemic antibody formation in the rat after intranasal administration of three different antigens. 191 2

Reciprocal transfers of spleen and bone marrow cell suspensions have been performed between mice of the C57BL/6 (B6) genetic background, differing at the lymphoproliferation (lpr) locus. These immune system chimaeras were followed for almost one year after sublethal irradiation and cell reconstitution. In addition to the survival of the chimaeras, the major lymphoid organs (bone marrow, spleen, thymus and lymph nodes) were examined for cell numbers, percentages of membrane immunoglobulin-positive cells and responses to mitogenic stimulations with concanavalin and lipopolysaccharide. The [lpr----lpr] chimaeras were similar to untreated lpr mice. The [wild----lpr] did not develop the lpr-induced syndrome and remained similar to [wild----wild] chimaeras. Therefore, B6 wild haematopoietic stem cells could rescue sublethally irradiated B6 lpr mice from the lpr-induced autoimmune pathology. The radioresistant lpr environment alone was not sufficient to induce the lpr syndrome. It may however be required for its development since [lpr----wild] chimaeras displayed a profound aplasia of their lymphoid organs, together with a normal cellularity of their bone marrow. In contrast to chimaeras constructed with MRL mice, the [lpr----wild] B6 chimaeras did not die following the lpr haematopoietic stem cell transfer. Therefore, the lymphoid aplasia of [lpr----wild] radiation chimaeras does not result from an lpr graft-versus-host-like syndrome. More likely is that a normal, non-lpr, haematopoietic environment may not allow the differentiation of the lpr haematopoietic stem cells into the lymphoid lineages.
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PMID:Reciprocal haematopoietic cell transfers between C57BL/6 mice differing at the lpr locus. 193 66

The homing of lymphoid cells to mucosa-associated lymphoid tissue is, amongst other factors, influenced by the nature of the antigen used to induce an immune response. To study this phenomenon we have monocolonized rats with a type 1 fimbriated Escherichia coli O6K13H1 strain and compared the secretory antibody response to colonization with the primary and secondary response obtained in rats immunized in the Peyer's patches (PP). Samples were tested with respect to the titres of antibodies against two antigens present on the E. coli strain: O6 lipopolysaccharide (LPS) and type 1 fimbrial antigen. In the primary immunized animals, IgA anti-fimbrial antibodies were mainly seen in milk and IgA anti-LPS antibodies mostly found in bile. In the booster immunized, and in the monocolonized, animals there was a shift of the antibody response towards the bile. Thus anti-fimbrial antibodies appeared in milk at approximately the same or at a lower level than in bile and the IgA anti-LPS antibodies were almost completely absent in the milk. The IgG antibody response of the animals immunized in the PP was primarily confined to milk for both anti-LPS and anti-fimbrial antibodies, while the colonized animals responded with higher levels in bile than in milk. IgM antibodies were only seen in the milk, except in primary immunized animals in which biliary IgM antibodies also were found. The data illustrate that: (i) primary stimulated cells predestined to produce IgA anti-LPS antibodies home mainly to the intestine, while cells predestined to anti-fimbrial antibody production have a greater tendency to populate the mammary gland; (ii) after repeated antigen stimulation and maturation of the immune response the cells are directed from the mammary gland to the intestine. We thus conclude that the nature of the antigen and the stage of lymphocyte maturation influences the homing of the cells and the appearance of various antibodies in different secretions.
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PMID:The secretory antibody response in milk and bile against fimbriae and LPS in rats monocolonized or immunized in the Peyer's patches with Escherichia coli. 197 93

Implantation of a 75-mg morphine pellet in sham-adrenalectomized male C3H/HeN mice resulted in significant elevations of serum corticosterone levels within 6 h. Corticosterone levels remained elevated (3- to 4-fold) for 72 h and had returned to normal by 120 h postimplantation. Within 48 h of pellet implantation, morphine-pelleted mice exhibited marked reductions in spleen (35%) and thymus weight (56%) relative to values in placebo-pelleted controls. In addition, adrenal hypertrophy was observed in the morphine-pelleted shams (50% increase in adrenal weight relative to placebo. The magnitude of splenic and thymic atrophy was reduced by about 50% in adrenalectomized morphine-pelleted mice (17% and 22% reductions, respectively) compared to that in adrenalectomized mice implanted with placebo pellets. Lymphocyte proliferative responses to the T-cell mitogen Concanavalin-A and the B-cell mitogen bacterial lipopolysaccharide were also significantly reduced in the morphine-pelleted sham mice. Morphine-induced suppression of Concanavalin-A- or lipopolysaccharide-stimulated lymphocyte proliferation was absent in adrenalectomized mice. Effects similar to adrenalectomy (e.g. lessening of magnitude of morphine-induced suppression of lymphoid organ weight and lymphocyte proliferation) were found in morphine-pelleted mice given the glucocorticoid receptor antagonist RU-486 at a dose of 10 mg/kg, twice daily. These studies imply that morphine-induced immunosuppression is at least in part mediated by the increase in serum corticosterone levels after implantation of the morphine pellet.
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PMID:Role of adrenal cortical activation in the immunosuppressive effects of chronic morphine treatment. 203 88

The minimal region of the human tumor necrosis factor alpha (TNF-alpha) gene promoter necessary for its transcriptional induction by phorbol esters (PMA) in human T and B lymphocyte cell lines has been localized between -52 and +89 nucleotides (nt) relative to the gene's transcriptional start site. Comparison of these sequences to those required to mediate virus or lipopolysaccharide (LPS) induction of the gene reveal significant differences, and thus, the sequence requirements for PMA induction are distinct from those that mediate induction by virus or LPS. Although three sites in the TNF-alpha promoter (kappa 1, kappa 2, and kappa 3) specifically bind the transcription factor NF-kappa B in lymphoid nuclear extracts, TNF-alpha mRNA induction by PMA does not correlate with NF-kappa B binding activities displayed by different T and B cell lines. Moreover, kappa 1-kappa 3 can each be deleted from the TNF-alpha promoter with little effect on the gene's inducibility by PMA. Therefore, TNF-alpha mRNA induction by PMA, like its induction by virus and LPS, is not primarily mediated by NF-kappa B, but rather is mediated through other sequences and protein factors. Surprisingly, multimers of kappa 1-kappa 3 can confer PMA inducibility on a heterologous promoter in a B (Raji), but not a T (HUT78) cell line. However they are not functional on a truncated TNF-alpha promoter, indicating that promoter context and cell type specificity influence the PMA inducible function of these NF-kappa B binding sites.
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PMID:Human tumor necrosis factor alpha gene regulation in phorbol ester stimulated T and B cell lines. 205 82

The cytokine interleukin-1 plays an important role in the production and modulation of the immune response in rheumatoid arthritis. It is produced by macrophages of the inflamed synovial tissue and induces the autocrine production of interleukin-1, amplifies the T-cell dependent immune response and has potent effects on inflammatory reactions of many non-lymphoid cell-systems. By means of a sensitive and specific ELISA interleukin(Il)-1 beta was measured in the peripheral blood and synovial fluid of patients with rheumatoid arthritis in comparison to controls in significantly increased levels (medium values: 280 pg/ml and 325 pg/ml versus less than 20 pg/ml). The Il-1 beta concentrations in the peripheral blood and in the synovial fluid were well correlated, but there was no correlation to other inflammation parameters like erythrocyte sedimentation rate or C-reactive protein, however, a good correlation to the nephelometrically measured rheumatoid factor (r = 0.71). In twelve hour cultures of adherent cells significantly increased spontaneous intracellular Il-1 beta-production was determined in synovial fluid macrophage cultures of rheumatoid arthritis patients compared to peripheral blood monocyte cultures of controls (median values 91.0 ng/10(6) cells versus 31.5 ng/10(6) cells). The secretion into the culture supernatant has to be stimulated by additional lipopolysaccharide. Interferon-gamma inhibits the spontaneous intracellular Il-1 beta-production of synovial fluid macrophages from rheumatoid arthritis patients. These findings may be of importance for the effect of the interferon-gamma therapy in the treatment of rheumatoid arthritis.
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PMID:[Interleukin-1 in the pathogenesis of chronic polyarthritis]. 211 62

B lymphocytes from the pulmonary lymphoid tissues were stimulated with a variety of thymus-independent (TI) antigens by intratracheal (i.t.) immunization. Immune responses in the lungs and hilar lymph nodes (HLN), which are part of the localized lymphoid tissue, as well as in the spleen, the systemic lymphoid organ, were studied. Thus, primary i.t. immunization of mice with the TI-1 antigen trinitrophenyl-lipopolysaccharide (TNP-LPS) elicited both antigen-specific and polyclonal plaque-forming cell responses from HLN, lung, and splenic B lymphocytes. These responses appeared as early as 3 days after immunization and declined by day 7. Similar immunization with another TI-1 antigen, TNP-Brucella abortus, resulted in anti-TNP responses in both pulmonary and systemic lymphoid tissues, although the kinetics of the antibody response were different than those to TNP-LPS. Interestingly an i.t. immunization with a TI-2 antigen, TNP-Ficoll, failed to induce an anti-TNP PFC response from HLN and lung B cells, although there was good antibody formation from splenic B cells. Antibody response to TNP-Ficoll was restored in pulmonary tissues when mice were immunized with TNP-Ficoll mixed with unconjugated B. abortus. In conclusion, our results indicate that TI-1 and TI-2 antigens differ in their ability to induce antibody responses in the pulmonary lymphoid tissues. The inability of TNP-Ficoll to elicit an antibody response in pulmonary lymphoid tissues has significance in the development of vaccines containing bacterial polysaccharides.
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PMID:Primary antibody responses to thymus-independent antigens in the lungs and hilar lymph nodes of mice. 211 56


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