Noverr Mairi C, Erb-Downward John R, Huffnagle Gary B
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109-0642, USA.
Clin Microbiol Rev. 2003 Jul;16(3):517-33. doi: 10.1128/CMR.16.3.517-533.2003.
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.
氧化脂质是脂肪酸的氧化代谢产物。类二十烷酸是氧化脂质的一个子集，包括前列腺素和白三烯，它们是宿主免疫反应的有效调节因子。宿主细胞是感染期间类二十烷酸和氧化脂质的一个来源；然而，类二十烷酸的另一个潜在来源是病原体本身。多种致病真菌、原生动物和蠕虫通过新的合成途径产生类二十烷酸和其他氧化脂质。这些生物体为什么会产生氧化脂质？越来越多的数据表明，这些生物体中的相变和分化受氧化脂质控制，包括前列腺素和脂氧合酶产物。病原体衍生的类二十烷酸在发病机制中的具体作用尚待确定，但病原体类二十烷酸与宿主中TH2反应发展之间的潜在联系很有趣。哺乳动物的前列腺素和白三烯已得到广泛研究，这些分子可以调节Th1与Th2免疫反应、趋化因子产生、吞噬作用、淋巴细胞增殖和白细胞趋化性。因此，类二十烷酸和氧化脂质（宿主或微生物来源）可能是宿主与病原体直接“对话”的介质，这种“对话”会促进慢性感染和超敏反应疾病，这是真核病原体感染的常见特征。
