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ARS Home » Pacific West Area » Davis, California » Western Human Nutrition Research Center » Immunity and Disease Prevention Research » Research » Publications at this Location » Publication #174887
Title: PLASMA CYTOKINIES AND OXIDATIVE DAMAGE IN HIV-POSITIVE AND HIV-NEGATIVE ADOLESCENTS AND YOUNG ADULTS: A PROTECTIVE ROLE FOR IL-10?

Author
item Stephensen, Charles
item MARQUIS, G - NUTR. DEPT. IOWA STATE
item DOUGLAS, S - CHILDRENS HOSPITAL, PA
item WILSON, C - PEDIATRICS, UNIV. AL

Submitted to: Trade Journal Publication
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/1/2005
Publication Date: 8/1/2005
Citation: Stephensen, C.B., Marquis, G.S., Douglas, S.D., Wilson, C.M. 2005. Plasma cytokinies and oxidative damage in hiv-positive and hiv-negative adolescents and young adults: a protective role for il-10. Trade Journal Publication.

Interpretive Summary: The cytokine IL-10 down-regulates certain aspects of an immune response. Since an active immune response can cause inflammation and oxidative damage, it has been proposed that IL-10 may have antioxidant properties as a result of diminished immune-activation. In the present study we found that HIV-positive adolescents and young adults with HIV infection that also had elevated IL-10 blood levels had lower levels of oxidative damage than did subjects with lower IL-10. This observation is consistent with the hypothesis that IL-10 may act as an anti-oxidant cytokine.

Technical Abstract: HIV infection causes immune activation that leads to oxidative damage. The regulatory cytokine IL-10 may protect against such damage. To examine this hypothesis, 67 cases of oxidative damage and 67 matched controls were selected from the Reaching for Excellence in Adolescent Health (REACH) study. Subjects were young (15 ' 23 y), largely female (76%), HIV-positive (73%) and black (69%). Plasma IL-10 had a significant, negative association with oxidative damage. This finding is consistent with a protective role for IL-10 in diminishing oxidative damage during immune activation.