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)

Abnormalities of lymphocyte proliferation in chronic hepatitis B virus infection are well documented, although the underlying mechanisms are poorly understood. To determine whether these defects may be secondary to disordered lymphokine production, we have simultaneously assayed interleukin-1 and interleukin-2 production in 31 chronic carriers of the hepatitis B virus. Supernatants from mononuclear cells cultured both in the presence and absence of lipopolysaccharide contained significantly increased quantities of interleukin-1 activity in patients compared with normal controls (p less than 0.01). Lysates of monocytes from patients also contained more interleukin-1 than those of controls (p less than 0.05) in the presence of lipopolysaccharide or silica, or both. These results indicate that interleukin-1 production is markedly elevated in patients with chronic hepatitis B virus infection, whereas in contrast, interleukin-2 production was found to be reduced in these patients (p less than 0.01). As one of the biological properties of interleukin-1 is to stimulate fibroblasts to produce collagen, the relationship between fibrosis in the liver biopsy specimen and interleukin production was examined. There was a highly significant correlation (p less than 0.001) between interleukin-1 production and the severity of fibrosis, suggesting that this lymphokine may be closely related to the development of cirrhosis in such patients.
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PMID:Interleukin-1 and interleukin-2 activity in chronic hepatitis B virus infection. 325 34

Alterations in the progression of the inflammatory disease in mice with established collagen-induced arthritis (CIA) by in vivo treatments with either anti-T cell antibodies or an immunosuppressive drug, whose main targets of action are T cells, were studied. It was demonstrated that the in vivo administration of either monoclonal anti-L3T4, anti-Ly-2 or the combination of anti-L3T4 and anti-Ly-2 failed to modify the inflammatory disease after the arthritis had been initiated. Nevertheless, the progression of disease was decreased by treatments with rabbit anti-mouse lymphocyte sera (ALS) in mice with established CIA. While there was a substantial reduction in the proliferative responses to the T cell mitogen concanavalin A (Con A) in these ALS-treated mice, proliferation to a B cell mitogen, lipopolysaccharide, was unaffected. Furthermore, treatments with anti-Thy-1.2 monoclonal antibody (mAb) by itself did not alter the progression of the ongoing inflammatory disease, but combined treatments with both anti-Thy-1.2 and anti-L3T4 mAb prevented the further advancement of the arthritic disease. Although mice receiving either anti-Thy-1.2 alone or both anti-Thy-1.2 and anti-L3T4 exhibited complete absence of Thy-1+ cells within their inguinal lymph nodes, the proliferative responses to Con A by LN cells from mice treated with the combination of anti-Thy-1.2 and anti-L3T4 were drastically reduced compared to the responses of either the anti-Thy-1.2 or anti-L3T4-treated groups. Finally, daily treatments with cyclosporin A, an immunosuppressive drug which preferentially acts on T cells, were also effective in modifying the clinical course of the arthritic disease in mice with established CIA. These results suggest that immunocompetent cells which express the Thy-1 surface marker, most likely Thy-1+ T cells, may play a role in maintaining and perpetuating the inflammatory disease of established CIA.
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PMID:The progression of the inflammation in established collagen-induced arthritis can be altered by treatments with immunological or pharmacological agents which inhibit T cell activities. 326 Jan 83

The formation of an air pouch in the subcutaneous tissues of a rat previously inoculated intradermally with Freund's mycobacterial adjuvant for the induction of arthritis, provokes a marked but transient inflammatory reaction in the cavity lining of the pouch. The dependence of this reaction on arthritis development was investigated. It was found that rats inoculated with mycobacterial adjuvant by subcutaneous or intraperitoneal injection failed to produce either a pouch reaction or develop arthritis. Intradermal injections of carrageenan, mycobacteria (M. tuberculosis in saline), Freund's incomplete adjuvant alone or containing Salmonella typhimurium lipopolysaccharide and Bordetella pertussis organisms or mycobacterial adjuvant containing egg albumin were also ineffective. Intradermal injections of type II collagen in Freund's incomplete adjuvant did induce arthritis but no pouch reaction; however, this could be elicited after direct challenge with antigen. Pretreatment of rats intraperitoneally with saline suspensions of mycobacteria or a moderate dose of cyclophosphamide prevented both the pouch reaction and arthritis developing to intradermal mycobacterial adjuvant. Pretreatment of rats with mycobacteria was without effect on type II collagen-induced arthritis. From the results of this study it would appear that the air pouch reaction and arthritis induced by adjuvant are directly associated. The inability of collagen to induce a similar reaction demonstrates a fundamental dissimilarity with mycobacterial adjuvant in its mechanism of production of arthritis.
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PMID:Polyarthritis and the air pouch reaction: dissimilarity of adjuvant and collagen models. 337 28

The in vitro production of anti-bovine type II collagen antibodies by lymphocytes from rats immunised with native bovine type II collagen and adjuvant was measured using a solid-phase enzyme-linked immunoassay. Antibodies to native bovine type II collagen could be detected in culture supernatants from the lymphocytes of rats only if they had been immunised with native bovine type II collagen, but not if immunised with native type I collagen, with keyhole limpet haemocyanin, with buffer or if un-immunised. The antibodies produced also bound to native rat, human and chick type II collagens, to native bovine 1 alpha 2 alpha 3 alpha collagen but not to native type I collagen. The amount of antibody in the cultures was altered by the presence of serum from type II collagen immunised rats or by the presence of either cyclohexamide, colchicine, Concanavalin A, catalase or lipopolysaccharide. Pre-treatment of the lymphocytes with mitomycin-C reduced the amount of anti-collagen antibody. This system can be used to investigate mechanisms controlling anti-collagen antibody production.
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PMID:Collagen-induced arthritis: antibody production by lymphocytes in vitro. 360 68

The effect of the migration of bovine blood polymorphonuclear leukocytes (PMNs) in vitro on their phagocytic activity was studied. PMNs were examined before and after migration through various membranes for rosette formation with sensitized sheep erythrocytes to detect Fc receptors (FcRs), phagocytic activity mediated through FcRs with opsonized staphylococci (Smith strain), and phagocytic activity mediated through nonimmunological receptors with unopsonized staphylococci (strain 305). Migration of PMNs was observed from the upper to the lower compartment of the blind well chamber through Millipore and Nuclepore membranes; through Millipore, Nuclepore, and nylon membranes coated with collagen; and through collagen-coated Millipore, Nuclepore, and nylon membranes overlaid with MA-104, BHK-21, MDBK-99, TB, or FBHE cells. Random migration of PMNs toward the plain medium (the same medium in the upper and lower compartments) through the membranes with and without a monolayer of cells increased the percentage of PMNs forming rosettes. In contrast, migration toward the medium containing lipopolysaccharide (LPS), formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP), or zymosan-activated serum (Act. serum) did not change the percentage of PMNs forming rosettes. The increased percentage of PMNs forming rosettes was associated with the enhanced phagocytosis of opsonized staphylococci (mediated by FcRs). In contrast, migration of PMNs toward LPS, FMLP, or Act. serum did not enhance phagocytosis mediated through FcRs. However, PMNs after migration toward LPS, FMLP, Act. serum, and plain medium enhanced phagocytosis of unopsonized staphylococci (mediated through the nonimmunological receptors).
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PMID:Appearance of Fc receptors on polymorphonuclear leukocytes after migration and their role in phagocytosis. 371 May 88

Peritoneal cells from thioglycollate-stimulated mice were allowed to adhere to coverglasses for 2 h to give a dense monolayer of adherent cells greater than 95% of which were macrophages. After incubation with the tetra-acetoxymethyl ester of quin2, coverglasses were rinsed with Ca2+-free saline, oriented at a 45 degree angle in square cuvettes containing a magnetically driven stir bar, and analyzed for changes in quin2 fluorescence in a spectrofluorimeter. Such fluorescence, taken as an indication of intracellular calcium ion concentration ([Ca2+]i), increased as exogenous calcium ion concentration ([Ca2+]o) was raised to 1 mM. At [Ca2+]o approximately equal to 10 microM, [Ca2+]i = 72 +/- 14 nM (n = 26); at [Ca2+]o = 1 mM, [Ca2+]i = 140-220 nM, levels not increased by N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine, a membrane-permeant chelator of heavy metals than can quench quin2. Addition of mouse alpha + beta fibroblast interferon, lipopolysaccharide, thrombin, collagen, vasopressin, ADP, compound 48/80, or U46619 did not change [Ca2+]i. However, addition of platelet activating factor (PAF) (2-20 ng/ml) raised [Ca2+]i by 480 nM within 1 min if [Ca2+]o = 1 mM. In the presence of 5 mM EGTA, PAF raised [Ca2+]i by 25 nM. This suggests that PAF causes influx of exogenous Ca2+, as well as releasing some Ca2+ from intracellular stores. Consistent with these results, when PAF was added to 1 mM Ca2+ in the presence of 100 microM Cd2+ or Mn2+ to block Ca2+ influx, [Ca2+]i increased by only intermediate amounts; at the times of such dampened peak response, [Ca2+]i could be raised within 1 min to normal PAF-stimulated levels by chelation of the exogenous heavy metals with diethylenetriaminepentaacetic acid. Normal PAF responses were observed in the presence of indomethacin. The lowest dose of PAF observed to raise [Ca2+]i was 0.1 ng/ml. Response of [Ca2+]i to 2-20 ng/ml PAF was transient, and second applications had no effect. The PAF response also was seen in cell suspensions. These results suggest that an increase in [Ca2+]i may be an early event in PAF activation of macrophages.
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PMID:Platelet activating factor raises intracellular calcium ion concentration in macrophages. 373 74

Interleukin-1 (IL-1) is a monocyte derived factor that participates in immune regulation and in the regulation of fibroblast proliferation and collagen deposition. It therefore, seems particularly pertinent to study in scleroderma, a disorder of immune regulation where increased collagen deposition is a hallmark. The production of IL-1 by lipopolysaccharide stimulated monocytes from 18 untreated scleroderma patients was akin to that of their normal matched controls. However, the unstimulated monocytes from six of the 18 scleroderma patients released IL-1 activity spontaneously into their supernatants. All six patients with spontaneous IL-1 release had less than 5 years disease duration. The response to IL-1 by T lymphocytes from patients with scleroderma was low as compared to those from controls. The presence of spontaneous IL-1 production with decreased response to IL-1 in scleroderma may indicate an in vivo pre-activation of monocytes to produce this factor that might have a bearing in the pathogenesis of collagen deposition in scleroderma.
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PMID:Spontaneous production of, and defective response to, interleukin-1 by peripheral blood mononuclear cells from patients with scleroderma. 387 55

The effect of parathormone (PTH), lipopolysaccharide (LPS), or interleukin-1 (IL-1) on calcium release and collagen degradation in bone was examined in vitro using labeled neonatal calvaria of normal mice and also of osteopetrotic microphthalmic (mi/mi) mice that have defective osteoclasts. All three agents stimulated calcium release from normal bone but not from mi/mi bone. PTH stimulated the degradation of both noncalcified and calcified collagen in normal bone as well as the degradation of noncalcified collagen in mi/mi bone. However, LPS and IL-1 only stimulated the degradation of calcified collagen in normal bone. One-half maximal stimulation of noncalcified collagen degradation in normal or mi/mi bone was achieved by about 3 nM PTH compared with about 1 nM PTH for that of calcium release from normal bone. While calcitonin (CT) and leupeptin inhibited calcium release and thereby the degradation of calcified collagen, neither agent inhibited PTH-stimulated noncalcified collagen degradation in normal or mi/mi bone. The data indicate the existence of two pathways that lead to collagen degradation in bone. One is intimately connected with the resorptive process stimulated by a variety of agents, and is probably mediated by osteoclasts. A second mechanism is sensitive only to PTH and appears to be associated with nonosteoclastic cells since it can operate under conditions in which osteoclasts are thought to be inactive or are inhibited.
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PMID:Evidence for two pathways for stimulation of collagenolysis in bone. 392 80

Two separate species of lipopolysaccharide (LPS) from Bacteroides gingivalis 381 have been isolated. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis demonstrated not only the heterogeneity of each species, but also that they represented high- and low-molecular-weight LPS entities. Although both contained the same carbohydrate and fatty acid components, the proportions of these differed between the LPS species. The direct effects of these two species in modulation of bone resorption and bone collagen and noncollagen protein synthesis have been examined. In a bone resorption assay, these two species stimulated 45Ca release from prelabeled fetal rat bones in a concentration range of 0.5 to 3.0 micrograms/ml. The two LPS species also elicited a 30 to 40% reduction in collagen protein formation at 10 micrograms/ml. Responses of the same order of magnitude were observed with LPS from Salmonella minnesota at 10 micrograms/ml. The higher-molecular-weight LPS species also significantly inhibited noncollagen protein formation. This is the first report that LPS from B. gingivalis 381, a suspected periodontal pathogen, inhibits bone collagen formation and, in conjunction with the bone resorption potency, further implicates LPS in alveolar bone loss associated with periodontal disease.
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PMID:Modulation of bone metabolism by two chemically distinct lipopolysaccharide fractions from Bacteroides gingivalis. 394 Sep 99

Time-lapse cinematography was used to study the chemotactic responsiveness of human blood lymphocytes as defined by morphological orientation and directional locomotion in gradients. At present, evidence for lymphocyte chemotaxis is indirect since neither of these essential features can be demonstrated with Boyden filter assays. Few lymphocytes direct from blood were motile, but culture in vitro for 1-3 days increased the proportion of locomotor forms to 30-40%. These cells were placed on 3-D collagen gels, and a chemotactic source was presented nearby on a small filter placed on the surface of, or within, the gel. The minority of lymphocytes that were capable of locomotion showed chemotactic responses to filters soaked in lipopolysaccharide if fresh human serum (20%), but not heat-inactivated serum, was present. Lymphocytes responded by protrusion of a lamella in the direction of the gradient source: 76% of locomotor lymphocytes showed their first orientation into the 180 degrees sector facing the source. They then moved directionally towards the source. The response to purified C5 peptides was equivocal. The locomotor lymphocytes showed a chemotactic response to supernatant fluids derived from cultures of the adherent mononuclear cell fraction from human blood (greater than 80% monocytes), judged by the same criteria. No particular lymphocyte type constituted the locomotor population. After exposure to LPS-activated serum, both T and B lymphocytes showed locomotor forms. There were slightly more T4+ cells among the locomotor population than among the population as a whole.
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PMID:A visual study of chemotaxis of human lymphocytes using a collagen-gel assay. 396 38


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