|Farnell, Morgan - TEXAS A&M UNIVERSITY|
|Lowry, Virginia - TEXAS A&M UNIVERSITY|
Submitted to: Society for Leukocyte Biology Meetings Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: November 9, 2001
Publication Date: N/A
Technical Abstract: Nitric Oxide (NO) is one of the end products of the metabolism of L- arginine to L-citrulline by nitric oxide synthase. It is a free radical with an unpaired electron, which reacts rapidly with molecular oxygen and oxygen radicals. It has both cytotoxic effects during inflammatory responses and regulatory effects as a component of physiological signaling transduction cascades. The cytotoxic effects require large amounts of NO and are an essential mechanism for control of invading microbes. The regulatory effects require much lower concentrations of NO. We quantified the production of nitrite, a stable metabolite of the NO pathway, in chicken macrophages, monocytes and heterophils after stimulation by IFNgamma, LPS and bacteria. Our results demonstrate that there is a differential activation of the NO pathway in each of these cell types. The tissue macrophage (HD-11) produced an average of 2.7 fold more nitrite (ugM) in comparison to peripheral blood monocytes and 27.7 fold more than peripheral blood heterophils. The minimal NO production by heterophils suggest that its primary purpose is regulatory not cytotoxic. Although heterophils have previously been demonstrated to be a major mechanism by which the innate immune system defends against microbial invasion, it would appear that control is accomplished via mechanisms other that NO production, such as oxidative burst and phagocytosis.