期刊
CLINICAL MICROBIOLOGY REVIEWS
卷 16, 期 3, 页码 517-+出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/CMR.16.3.517-533.2003
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资金
- NHLBI NIH HHS [R01 HL065912, R01-HL63670, R01-HL65912] Funding Source: Medline
- NIAID NIH HHS [T32 AI007528, T32AI07528] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
Oxylipins are oxygenated metabolites of fatty acids. Eicosanoids are a subset of oxylipins and include the prostaglandins and leukotrienes, which are potent regulators of host immune responses. Host cells are one source of eicosanoids and oxylipins during infection; however, another potential source of eicosanoids is the pathogen itself. A broad range of pathogenic fungi, protozoa, and helminths produce eicosanoids and other oxylipins by novel synthesis pathways. Why do these organisms produce oxylipins? Accumulating data suggest that phase change and differentiation in these organisms are controlled by oxylipins, including prostaglandins and lipoxygenase products. The precise role of pathogen-derived eicosanoids in pathogenesis remains to be determined, but the potential link between pathogen eicosanoids and the development of TH2 responses in the host is intriguing. Mammalian prostaglandins and leukotrienes have been studied extensively, and these molecules can modulate Th1 versus Th2 immune responses, chemokine production, phagocytosis, lymphocyte proliferation, and leukocyte chemotaxis. Thus, eicosanoids and oxylipins (host or microbe) may be mediators of a direct host-pathogen cross-talk that promotes chronic infection and hypersensitivity disease, common features of infection by eukaryotic pathogens.
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