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* Department of Experimental Pathology, Institute of Medical Biology, University of Tromsø, Norway
Department of Evolutionary Immunobiology, Institute of Zoology, Jagiellonian University, Krakow, Poland
Correspondence: Barbara Plytycz, Department of Evolutionary Immunobiology, Institute of Zoology, Jagiellonian University, R. Ingardena 6, PL-30-060 Krakow, Poland. E-mail: plyt{at}zuk.iz.uj.edu.pl
Zymosan-induced peritonitis was investigated in mast cell-deficient
WBB6F1 mice and in Balb/c mice pretreated with mast cell stabilizer
(cromolyn) or antagonists of histamine receptors (mepyramine,
triprolidine, cimetidine, or ranitidine). The inherited mast cell
deficiency in W/Wv knockouts of WBB6F1 mice impaired
significantly the level of histamine and plasma exudation (measured 30
min after stimulation) as well as the influx of exudatory leukocytes,
accumulation of plasma and exudate chemoattractants, and the release of
proinflammatory cytokines (TNF-
, IL-1ß, and IL-6) measured at
6 h of inflammation. All of those factors were fully restored
after selective intraperitoneal reconstitution of W/Wv mice
with bone marrow-derived mast cells from their control +/+
counterparts. Cromolyn pretreatment of Balb/c mice reduced exclusively
the early plasma exudation and histamine influx. Blocking of histamine
receptors inhibited not only the early plasma exudation but also
temporarily diminished primary leukocyte influx and levels of MCP-1 and
IL-1ß. In conclusion, mast cells play an important role in the
initiation of zymosan-induced peritonitis and modulate its further
course.
Key Words: peritonitis • cromolyn • mepyramine • histamine receptors • exudate leukocytes
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