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)

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

Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, which is associated with high mortality and long-term cognitive impairment even when effective anti-parasitic treatment is administered. (1 , 2) Supportive therapy is needed to improve both morbidity and mortality associated with this condition. In an accompanying paper, we have demonstrated that in the Plasmodium berghei ANKA (PbA) rodent model, CM can be effectively prevented by a treatment combining sub-lethal doses of lipopolysaccharide S (LPS) and vascular endothelial growth factor (VEGF). Since LPS is not suitable for human therapy, we investigated whether lovastatin would represent a suitable substitute. This compound, widely used to lower cholesterol levels in plasma, shares with LPS the ability to elicit an anti-inflammatory response by activating the Nrf-2 gene, and when given to P. berghei-infected mice prevents to some extent the onset of CM. We show here that lovastatin- and VEGF-treated mice did not develop CM and showed few signs, if any, of endothelial damage and systemic inflammation. The combination treatment was much more effective than lovastatin and VEGF alone. Immunohistochemistry and gene expression analysis indicated that VEGF and LPS together overturned the two pathogenic mechanisms responsible for the development of CM: endothelial damage and disregulated activation of the inflammatory response. These findings provide the rationale for investigating the therapeutic potential of these compounds in human CM as well as in other inflammatory pathologies that respond poorly to steroid and non-steroid anti-inflammatory therapy.
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PMID:Vascular endothelial growth factor (VEGF) and lovastatin suppress the inflammatory response to Plasmodium berghei infection and protect against experimental cerebral malaria. 2647 2