Candida Oxylipins as A Source for Human Respiratory Inflammation

Byron's Comments:

An overgrowth of Candida can communicate to the human genome and create excessive inflammatory and allergic responses anywhere in the body.

Study Title:

Production of Eicosanoids and Other Oxylipins by Pathogenic Eukaryotic Microbes

Study Abstract:

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.

Study Information:

Mairi C. Noverr, John R. Erb-Downward, and Gary B. Huffnagle. Production of Eicosanoids and Other Oxylipins by Pathogenic Eukaryotic Microbes Clinical Microbiology Reviews 2003 July 517-533, Vol. 16, No. 3
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan 48109-06422

Full Study:

http://cmr.asm.org/cgi/content/full/16/3/517

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