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)

Phagocytosis of Giardia lamblia trophozoites by cytokine-activated and non-activated bone marrow-derived macrophages was examined in vitro. Macrophages treated with recombinant interferon-gamma (IFN-gamma) and bacterial lipopolysaccharide (LPS) ingested a significantly higher number of in vitro-grown trophozoites than untreated macrophages. Maximal uptake of parasites occurred after 4 h and 6 h of incubation where 81.4% and 79.1% of macrophages were positive for trophozoites. Other cytokines tested, IL-2, IL-3, IL-4, IL-5, GM-CSF, CSF-1 and tumour necrosis factor-alpha (TNF-alpha) either alone or in combination with LPS, failed to activate macrophages to phagocytose G. lamblia. The induction of this activated macrophage anti-microbial function was achieved pharmacologically using phorbol myristate acetate (PMA) and ionophore A23187. The giardicidal activity of macrophages activated with IFN-gamma and LPS or that induced by PMA and A23187 was inhibited by H-7, indicating the role for protein kinase C in the intracellular events following activation.
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PMID:Phagocytosis of Giardia lamblia trophozoites by cytokine-activated macrophages. 173 94

Macrophages derived in vitro from bone marrow progenitors (bone marrow-derived macrophages, BMDMs) using either macrophage colony-stimulating factor (CSF-1) or granulocyte-macrophage colony-stimulating factor (GM-CSF) as the myelopoietic stimulus display differential functional, morphological, and mRNA phenotypes. The data presented here demonstrate further that CSF-1- and GM-CSF-derived BMDMs differ in immunologic capacity. GM-CSF-derived BMDMs, when compared to CSF-1-derived BMDMs, showed greater cytolytic activity against tumor necrosis factor alpha (TNF-alpha)-resistant, but not TNF-alpha-sensitive, tumor targets. In contrast, CSF-1-derived BMDMs produced nitrite in response to lipopolysaccharide (LPS) alone, whereas GM-CSF-derived BMDMs required interferon gamma plus LPS treatment. The two BMDM populations also showed differential sensitivities to LPS for secretion of TNF-alpha and nitrite, but the maximal inducible amounts of these factors and prostaglandin E2 were similar between the BMDM populations. Lastly, GM-CSF-derived but not CSF-1-derived BMDMs showed an L-arginine-dependent listeriacidal activity. These results show that the functional heterogeneity of CSF-1- and GM-CSF-derived macrophages is limited and appears to result largely from differences in the activational signals required by each BMDM population to elicit a given function.
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PMID:Differential immunocompetence of macrophages derived using macrophage or granulocyte-macrophage colony-stimulating factor. 174 Jun 46

Treatment of fresh non-adherent bone marrow cells (NABMC) with cisplatin or lipopolysaccharide (LPS) did not render them tumoricidal. NABMC incubated in medium alone or medium containing recombinant granulocyte macrophage colony stimulating factor (rGM-CSF) for 4 days matured to macrophages that were positive for non-specific esterase staining. Bone marrow-derived macrophages cultured with medium alone did not respond to cisplatin or LPS by the induction of tumoricidal activity, whereas rGM-CSF derived bone macrophages showed significantly enhanced cytotoxicity after treatment with cisplatin or LPS. Culturing of NABMC with rGM-CSF enhanced cell survival compared to the cells incubated in medium alone. These results suggest that bone marrow cells not only mature in rGM-CSF, but are also primed by rGM-CSF for induction of tumoricidal activity.
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PMID:In vitro activation of rGM-CSF derived bone marrow macrophages by cisplatin and lipopolysaccharide. 178 94

Members of the beta 1 subfamily of integrins, a group of heterodimeric transmembrane adhesion receptors, mediate the attachment of monocytes and macrophages to cell matrix proteins such as fibronectin, collagen, and laminin. Such interactions are likely of considerable importance during inflammatory responses, when monocytes are recruited to, and retained in, extravascular sites. Because of the complexity of the interactions that befall monocytes during an inflammatory response, it seems likely that expression of adhesion receptors on monocytes would be precisely regulated. In the present study, we have examined the mRNA expression of alpha 5 and beta 1 subunits of the fibronectin receptor in purified human peripheral blood monocytes and monocyte-derived macrophages cultured in the absence or presence of various agents known to induce activation and/or differentiation. Incubation under nonadherent conditions for 6 h with interferon (IFN)-gamma or bacterial lipopolysaccharide (LPS) resulted in a decreased expression of both alpha 5 and beta 1 mRNAs in freshly isolated monocytes. In contrast, incubation with IFN-alpha did not result in a decreased expression of alpha 5 mRNA, although a moderate decrease in beta 1 mRNA was observed. Culture with granulocyte-macrophage colony-stimulating factor, macrophage colony-stimulating factor, phorbol myristic acetate, or plasma fibronectin (under nonadherent and adherent conditions) did not result in a change in levels of alpha 5 or beta 1 transcripts. In contrast to the results obtained with freshly isolated monocytes, incubation for 6 h with IFN-gamma or LPS did not alter the expression of alpha 5 or beta 1 mRNA in macrophages derived by culture of monocytes for 6 days in Teflon beakers. Our results indicate that IFN-gamma and LPS, both of which may be present in inflammatory sites, downregulate the mRNA expression of fibronectin receptor subunits in monocytes. Moreover, alpha 5 and beta 1 gene regulation by these agents is apparently dependent on the differentiation stage of the cells. This may provide a mechanism by which extravasating monocytes detach from extracellular matrix proteins, present in subendothelial basement membranes and deposited in sites of inflammation, in order to pursue other activities.
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PMID:Regulation of fibronectin receptor (alpha 5 beta 1) mRNA expression in human monocytes and monocyte-derived macrophages by activation/differentiation signals. 183 43

Intraperitoneal injection of Streptococcus agalactiae sonicated cells into Wistar rats causes a chronic relapsing polyarthritis resembling human rheumatoid arthritis. We report evidence favoring a role for macrophages in the pathology of this disease. S. agalactiae injected ip induced a high level of tumor necrosis factor release by peritoneal macrophages isolated subsequently, and had a similar effect when added to control peritoneal macrophages in culture. Ia antigen was induced on macrophages in both the peritoneum and affected joints following S. agalactiae injection. The role of macrophages in the disease process was studied by treating animals prior to S. agalactiae injection with varying concentrations of bacterial lipopolysaccharide (LPS), silica, and carrageenan, agents known to have a biphasic effect on macrophage function. They aggravated the pathology at low doses but prevented the disease at high doses. The most specific alteration of macrophage levels was achieved by injection of recombinant human macrophage colony-stimulating factor (CSF-1). Treatment with CSF-1 early in the disease lead to significant worsening of the pathology. Administration of CSF-1 after 2 weeks reactivated the disease and extended the chronic phase. These data in combination with previous findings are consistent with nonimmune, macrophage-mediated pathology for this model of arthritis. The results have implications for therapeutic application of CSF-1.
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PMID:The role of macrophages in experimental arthritis induced by Streptococcus agalactiae sonicate: actions of macrophage colony-stimulating factor (CSF-1) and other macrophage-modulating agents. 187 58

We have shown that certain murine tumors grow more slowly and spread less readily in immune deficient animals. We have also demonstrated that immunologic factors explain certain aspects of this difference. In the work presented we demonstrate that a subpopulation of splenocytes produce a factor(s) that enhances tumor cell proliferation in vitro. We also describe an in vitro model to determine the level of tumor stimulatory activity. We found that the tumor cell growth-enhancing activity (TEA) is heat stable but sensitive to trypsin digestion, low pH and beta-mercaptoethanol. TEA production is found to be insensitive to mitogen stimulation such as concanavalin A, lipopolysaccharide, and phytohemagglutinin. Among the known growth factors and interleukins we have tested (interleukin 1-7, basic FGF, EGF, TGF-beta PDGF, GM-CSF, and MCSF), none appear to account for TEA activity.
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PMID:Initial description of a tumor enhancing activity produced by murine splenocytes. 188 89

In addition to its hematopoietic activities, interleukin-3 (IL-3) can modulate macrophage functions. We have studied the production of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor (TNF) by mouse peritoneal macrophages triggered by lipopolysaccharide (LPS) in the presence or absence of IL-3. Interleukin-3 at the concentration used (i.e., 100 U/ml) did not induce the production of any cytokines, whereas it enhanced significantly the secretion of IL-1, IL-6 and TNF by LPS-stimulated macrophages. The synergistic activity of IL-3 was observed over a wide range of Escherichia coli or Salmonella enteritidis LPS concentrations. No additive effect was noticed between IL-3 and granulocyte/macrophage colony-stimulating factor (GM-CSF), another factor able to enhance LPS-induced IL-1 production. Thus, IL-3 can potentiate the inflammatory response induced by endotoxin from Gram-negative bacteria through a potentiation of cytokine production.
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PMID:Interleukin-3 enhances cytokine production by LPS-stimulated macrophages. 188 10

Peritoneal macrophages from BALB/c mice after treatment for 24 h in vitro with cisplatin, lipopolysaccharide (LPS) or mitomycin-C were rendered significantly cytotoxic against L-929 tumor target cells. In a similar experiment none of these agents could induce tumoricidal activity of fresh non-adherent bone marrow cells (NABMC). NABMC when incubated in medium alone or in medium containing L-929 culture medium (L-929 CM), a form of macrophage colony stimulating factor (M-CSF), for three days matured to macrophages which were positive for non-specific esterase staining. These bone marrow-derived macrophages cultured with medium alone did not respond to cisplatin. LPS or mitomycin-C for induction of tumoricidal activity whereas bone marrow derived macrophages with that were incubated with L-929 CM showed also significantly enhanced cytotoxicity after treatment with cisplatin, LPS and mitomycin-C. Culturing of NABMC with L-929 CM significantly enhanced cell survival as compared to the cells incubated in medium alone. These results suggest that bone marrow cells not only mature in L-929 CM but also are primed by L-929 CM for induction of tumoricidal activity.
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PMID:In vitro activation of murine bone marrow-derived macrophages with cisplatin and mitomycin-C. 190 38

The production of colony-stimulating factors (CSFs) by murine bone marrow stromal cells was studied with Dexter long-term bone marrow culture (LTBMC). For induction of CSF release, various concentrations (0.5-40.0 microgram/ml) of bacterial lipopolysaccharide (LPS) were added to nonrecharged 3-week-old LTBMCs consisting of an intact or macrophage-depleted adherent cell layer. The depletion of monocytes/macrophages from freshly prepared bone marrow cell suspension was performed by carbonyl-iron incorporation before establishment of LTBMC. The supernatants (Sup) of normal LTBMCs contained a low level of macrophage colony-stimulating factor (M-CSF) that was produced by the adherent cells but not by the nonadherent cell elements. No colony inhibitor was found in the Sup of LTBMCs, whereas a colony-promoting activity (CPA) was detected in medium conditioned by the adherent marrow cells (AC-CM). CPA could enhance the colony formation of myeloid progenitor cells when used in combination with recombinant murine granulocyte-macrophage colony-stimulating factor (GM-CSF). The production of CSFs peaked at about 24 h after refeeding, but it then declined to only half the optimal activity at the end of the week. Addition of LPS to the intact LTBMC invariably increased the production of a GM-CSF-like cytokine. The release of this cytokine was dose dependent and peaked at a dosage of 20 micrograms/ml of LPS at 24 h after treatment. In contrast, macrophage-depleted marrow-adherent cells failed to respond to LPS for CSF secretion. These results suggest that LPS can stimulate marrow macrophages to directly release CSF or to potentiate the production of CSF by other stromal cells.
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PMID:Effect of lipopolysaccharide on the production of colony-stimulating factors by the stromal cells in long-term bone marrow culture. 199 94

Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting.
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PMID:Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes. 199 52


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