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Population kinetic study of guinea pig monocytes and their subsets during acute inflammation
Authors:S J Normann  S J Noga
Institution:1. Department of Aerospace and Mechanical Engineering, University of Southern California, Los Angeles, CA 90089, USA;2. Sandia National Laboratories, PO Box 5800-1056, Albuquerque, NM 87185, USA;3. Department of Chemical Engineering and Materials Science, University of Southern California, 3650 McClintock Ave., Los Angeles, CA 90089, USA;1. University of Brescia, Department of Mechanical and Industrial Engineering, via Branze 38, 25124 Brescia, Italy
Abstract:Guinea pig peripheral blood monocytes exist in four subsets which differ in cytochemistry, function, rates of production, and circulatory time during steady state. These subsets are designated small, intermediate, large, and very large vacuolated monocytes. To address the question as to whether all subsets participate equally in the acute inflammatory response, population kinetics were performed on monocyte subsets isolated by counterflow centrifugation elutriation following a single intravenous pulse of tritiated thymidine given concurrently with an intraperitoneal injection of phytohemagglutinin as phylogistic agent. Inflammation reduced the cell cycle times of the precursors for all monocyte subsets, increasing their production. However, inflammation increased the number of precursors only for large monocytes. In addition, a reserve of exclusively large monocytes existed which appeared in the circulation within 3 hr of inflammation induction. The subsequent loss of large monocytes from the circulation exceeded their production in contrast to all other monocyte fractions. Over 92% of all monocytes entering the acute inflammatory site were large monocytes despite the fact that they constituted only 58% of monocytes under steady state conditions. Small, intermediate, and very large vacuolated monocytes were only minor participants in the acute inflammatory response. These results indicate heterogeneity in the monocyte subset response to acute inflammation.
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