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Can diesel particulate matter directly activate cardiac mast cells?
Author(s) -
Gardner Jason D.,
Murray David B,
Morgan Loren G,
Carpenter Christin L,
Bradshaw Joseph B,
Brower Gregory L
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1140
Subject(s) - histamine , mast cell , chemistry , secretagogue , pharmacology , endocrinology , immunology , biochemistry , medicine , secretion
Rats subjected to inhaled diesel exhaust particles (DEP) developed a significant reduction in cardiac function. Histological examination of their hearts demonstrated a significant increase in cardiac mast cell (CMC) density coupled with increased matrix metalloproteinase activity. Pretreatment with a mast cell stabilizing compound prevented these effects on cardiac function indicating that they were mast cell‐mediated. However, it was not clear if this mast cell activation was the result of a direct interaction of DEP with CMCs. The purpose of this study was to determine if DEP can directly activate CMCs. CMCs were isolated from rats and exposed to DEP or the mast cell secretagogue 48/80. 48/80 treatment triggered a significant histamine release above that of controls (80.5% and 26.1% of total histamine, respectively). However, exposure to DEP did not result in histamine release above that seen in controls (26.8%). Retained histamine levels were comparable for the control and DEP‐exposed cells, ~50 ng/ml. These findings indicate that the DEP effects on cardiac function are not due to a direct action of DEP on CMCs. However, given the ability of endothelin‐1 (ET‐1) to stimulate mast cell activation in the whole heart and peritoneal mast cells, a DEP‐induced ET‐1 release from the lungs and subsequent paracrine activation of CMCs represents a plausible mechanism. Support: AHA 0435298N (JDG), EPA RD‐83195301‐0 (GLB)