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Controls Neutrophil Migration Across the Mesothelium In Vitro and In Vivo1
*
Institute of Nephrology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom;
Theodor Kocher Institute, University of Bern, Bern, Switzerland; and
Cardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom
Leukocyte recruitment into the infected peritoneal cavity consists
of an early, predominant polymorphonuclear leukocyte (PMN) influx and
subsequent, prolonged mononuclear cell migration phase. Although
chemokine secretion by resident peritoneal cells plays a primary role
in mediating this migration, the mechanisms involved in controlling the
switch in phenotype of cell infiltrate remain unclear. The present
study investigates a potential role for the Th1-type cytokine IFN-
in the process of leukocyte recruitment into the peritoneal cavity.
Stimulation of cultured human peritoneal mesothelial cells with IFN-
(1–100 U/ml) alone or in combination with IL-1
(100 pg/ml) or
TNF-
(1000 pg/ml) resulted in significant up-regulation of monocyte
chemoattractant protein-1 and RANTES protein secretion. In contrast,
IFN- inhibited basal and IL-1-, and TNF--induced production of
IL-8. The modulating effects of IFN- on chemokine production
occurred at the level of gene expression, and the degree of regulation
observed was dependent on the doses of IL-1 and TNF- used.
Analysis of the functional effects of IFN- on IL-1-induced
transmesothelial PMN migration with an in vitro human transmigration
system and an in vivo murine model of peritoneal inflammation
demonstrated that IFN- was able to down-regulate PMN migration
induced by optimal doses of IL-1. These effects were mediated in
vivo via down-regulation of CXC chemokine synthesis. These findings
suggest that IFN- may play a role in controlling the phenotype of
infiltrating leukocyte during the course of an inflammatory response,
in part via regulation of resident cell chemokine
synthesis.
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