SEQUESTRATION PATTERNS OF TRANSFUSED RAT NEUTROPHILIC GRANULOCYTES UNDER NORMAL AND INFLAMMATORY CONDITIONS

Citation
K. Lovas et al., SEQUESTRATION PATTERNS OF TRANSFUSED RAT NEUTROPHILIC GRANULOCYTES UNDER NORMAL AND INFLAMMATORY CONDITIONS, European journal of haematology, 56(4), 1996, pp. 221-229
Citations number
31
Categorie Soggetti
Hematology
ISSN journal
09024441
Volume
56
Issue
4
Year of publication
1996
Pages
221 - 229
Database
ISI
SICI code
0902-4441(1996)56:4<221:SPOTRN>2.0.ZU;2-B
Abstract
The fate of polymorphonuclear neutrophilic granulocytes (PMN) after th eir mobilization from the bone marrow of healthy individuals is not cl early understood. It has been suggested that there is a continuous uti lization of these cells in widespread, subclinical inflammatory foci, where they are ultimately degraded. The goal of the present experiment s was to determine whether an alternative ecotaxis (''homing'') exists , namely sequestration and degradation of PMN by mononuclear phagocyte s exposed to the bloodstream in the liver, spleen and bone marrow. Blo od PMN were collected from donor rats, labelled with Cr-51, and inject ed i.v. into 2 syngeneic rats, one of them having an induced sterile p eritonitis. After various time intervals up to 18 h, the rats were kil led and exsanguinated. As expected, we found cell-bound radioactivity in the inflamed peritoneal cavities, and also a high amount of radioac tivity in liver, spleen, and bone marrow. The bone marrow uptake of PM N appeared to be much lower in the inflammation rats than in the norma l controls. These findings were confirmed in PMN transfer experiments using PVG rats congenic for the RT7 alloantigenic system. Here, transf used blood leukocytes were traced with fluorescent, monoclonal HIS41 a ntibodies and how cytometry. A possible corticosteroid effect on the b one marrow sequestration could not be substantiated. Uptake and degrad ation of PMN takes place in organs containing phagocytes exposed to th e bloodstream. Sequestration of PMN in the bone marrow is apparently d own-regulated in inflammatory states, perhaps increasing the PMN avail ability to inflamed tissue.