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)

Addition of small amounts of chromium chloride to a saline suspension of Salmonella typhosa lipopolysaccharide (LPD; Difco) caused a marked reduction in several of the biologic activities of this substance including toxicity, B-cell mitogenicity, plasma colony-stimulating activity (CSA), radioprotective effect, and induction of the dermal Shwartzman reaction. Nevertheless, LPS treated with chromium chloride was found to be at least as effective as untreated LPS in enhancing resistance of B6CBF1 mice to the lethal effects of Klebsiella pneumoniae infection.
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PMID:Biologic properties of bacterial lipopolysaccharides treated with chromium chloride. 35 Mar 61

In vitro and in vivo responses to lipopolysaccharide (LPS) and various other bacterial immunostimulants were compared in c3H/He low-responder mice. The principal findings were as follows. (i) Their splenic lymphocytes were stimulated by various gram-negative mitogens such as an Escherichia coli peptidoglycan, a detoxified derivative of LPS, and even endotoxins extracted by trichloroacetic acid that are known to contain protein; spleen cells of these mice were also transformed by two other B-cell mitogens extracted from acid-fast organisms. (ii) Their macrophages were refractory to LPS and weakly responsive to a mycobacterial prepartion. (iii) LPS failed to elicit nonspecific resistance in these mice against Klebsiella pneumoniae infection. (iv) Endotoxin extracted by trichloroacetic acid and a mycobacterial preparation that could increase nonspecific resistance to infection in other strains did not protect C3H/He mice against a challenge by K. pneumoniae, although both prepartions could evoke nonspecific responses of B cells in this low-responder subline.
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PMID:Failure of endotoxin to increase nonspecific resistance to infection of lipopolysaccharide low-responder mice. 77 22

In a previous study, we demonstrated that lipopolysaccharide (LPS) and other bacterial immunostimulants, in contrast to their activity in a closely related high-responder subline, failed to elicit nonspecific resistance in LPS low-responder mice against Klebsiella pneumoniae infection. To investigate the type of inheritance controlling the LPS-induced nonspecific resistance to infection, the present study was performed in low- and high-responder C3H sublines and in F1 and F2 hybrids. In addition, F1 mice were backcrossed to each parental type. Inheritance of susceptibility to endotoxin was also tested in both sublines and their hybrids and backcross progeny. For these latter assays, mice were previously adrenalectomized because removal of this gland considerably enhances their sensitivity. Our present findings are consistent with the hypothesis that LPS enhances nonspecific resistance to infection and that susceptibility to endotoxin shock in the absence of corticoids may be determined by a single autosomal dominant gene.
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PMID:Inheritance of lipopolysaccharide-enhanced nonspecific resistance to infection and of susceptibility to endotoxic shock in lipopolysaccharide low-responder mice. 86 9

Dietary fish-oil supplementation interferes with eicosanoid production and appears to decrease production of interleukin-1 (IL-1) and tumor necrosis factor (TNF). The effect of fish oil was investigated in an intramuscular Klebsiella pneumoniae infection in Swiss mice and in cerebral malaria induced by Plasmodium berghei in C57B1/6 mice. After a low inoculum of K. pneumoniae, 90% of fish oil-fed mice survived; survival in control mice fed equal amounts of corn or palm oil or normal chow was 30%, 40%, and 0, respectively. Cerebral malaria occurred in only 23% of fish oil-fed mice; in the controls, cerebral malaria developed in 61%, 81%, and 78%, respectively. Contrary to what was expected, lipopolysaccharide-induced ex vivo production of IL-1 alpha and TNF alpha by peritoneal cells was significantly enhanced in fish oil-fed mice compared with controls. Indomethacin treatment did not alter the outcome in these two infections, thus arguing against reduced prostaglandin synthesis as an explanation for the increase in resistance to infection.
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PMID:Dietary fish-oil supplementation in experimental gram-negative infection and in cerebral malaria in mice. 156 40

The ability of aporphinoid alkaloid oxoglaucine to influence T- and B-cell immune response was studied in mice models. The substance inhibited in vitro mitogen-induced lymphocyte proliferation and suppressed antibody response to sheep red blood cells (SRBC) and lipopolysaccharide (LPS) in vivo effectively. The action depended on the relative timing of antigen and oxoglaucine administration. The substance manifested stimulatory effect in popliteal lymph node (PLN) reaction and LPS-induced B-cell activation. In the chronic inflammatory model of adjuvant arthritis oxoglaucine exhibited stimulatory or suppressive action related to the kinetics of the process. At low doses (1 or 2 mg kg-1) oxoglaucine improved the outcome of Klebsiella pneumoniae infection, while at higher doses (10 or 20 mg kg-1) the substance caused an impairment of host resistance to infectious agent. The comparison with cyclophosphamide in some tests showed that oxoglaucine was effective in manifold lower doses. In conclusion, oxoglaucine exerted immunomodulatory effects in vivo in a dose-dependent and protocol-dependent manner. Yet, its overall action might be attributed to the different sensitivity of the cells involved in the developing immune response.
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PMID:Immunopharmacological activity of aporphinoid alkaloid oxoglaucine. 926 41