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Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:1954-1961

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:1954-1961.)
© 1997 American Heart Association, Inc.

Articles

Cytokine Modulation of LDL Oxidation by Activated Human Monocytes

Virginia A. Folcik; Rozina Aamir; ; Martha K. Cathcart

From the Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio.

Correspondence to Martha Cathcart, PhD, Department of Cell Biology, Building NC1, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail cathcam{at}cesmtp.ccf.org

Abstract There is considerable evidence to suggest that cytokines modulate the pathological cellular events that occur in human atherosclerosis. We sought to determine the effects of T-helper-lymphocyte (TH)-1- and TH2-type cytokines on the ability of human monocytes to oxidize LDL, one of the pathological processes believed to occur in atherosclerosis. The ability of opsonized zymosan (ZOP)-activated human monocytes to oxidize LDL in a 24-hour period was significantly enhanced by pretreatment of the monocytes with the TH2 cytokines, interleukin (IL)-4, or IL-13 compared with untreated monocytes. In contrast, interferon (IFN)-{gamma}, a TH1 cytokine, inhibited LDL oxidation by activated monocytes. Treatment with IFN-{gamma} also prevented the IL-4- and IL-13-mediated enhancement of LDL oxidation by ZOP-activated monocytes. Untreated or cytokine-treated unactivated monocytes did not oxidize LDL. The enhancement of LDL oxidation mediated by IL-4 or IL-13 treatment was not due to a mitogenic effect of the cytokines on the monocytes, nor to modulation of superoxide anion (O2-) production. The cytokine regulation of 15-lipoxygenase (LO) in the monocytes was also examined. IL-4 and IL-13 induction of 15-LO mRNA and 15-LO activity in the monocytes was confirmed, as was the previously reported inhibition of induction by IFN-{gamma}. In summary, IL-4 and IL-13 enhance the ability of activated human monocytes to oxidize LDL, whereas IFN-{gamma} inhibits the cell-mediated oxidation. The up- and downregulation of activated monocyte-mediated LDL oxidation by these cytokines correlates with the expression of 15-LO activity. Considerable evidence suggests that the progression of atherosclerosis includes events that are immunologically mediated, lending potential physiological relevance to these in vitro observations.


Key Words: cellular activation • cytokines • human • monocytes • macrophages • LDL




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