Tobacco smoke releases performed mediators from canine mast cells and modulates prostaglandin production.
The role of an extract of tobacco smoke in activating mast cells was studied. With the use of isolated, canine mast cells as a model, we found that cigarette smoke solution (CSS) induced the release of the performed mediators histamine and tryptase from these cells in an energy- and temperature-dependent, non-cytotoxic manner. There was no requirement for extracellular calcium. Nicotine tartrate did not reproduce the effect of CSS. Interestingly, mast cells produced little prostaglandin D2 (PGD2) in response to the CSS, and there was a concentration-related inhibition of calcium ionophore A23187-induced PGD2 synthesis. This suggests at least two mechanisms acting on the mast cell: tobacco smoke can directly activate mast cells to release performed mediators and can simultaneously inhibit prostaglandin production. These observations suggest a mechanism by which mast cells may participate in the bronchospastic and proinflammatory changes seen in the lungs and airways of smokers.
Thomas
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PS
Cardiovascular Research Institute, University of California, San Francisco 94143.
Schreck
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RE
Lazarus
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SC
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002470:Cell Survival; D004285:Dogs; D004734:Energy Metabolism; D008407:Mast Cells / Q000378:metabolism*; D009538:Nicotine / Q000494:pharmacology; D010947:Plants, Toxic; D015230:Prostaglandin D2 / Q000096:biosynthesis*; D012906:Smoke; D012996:Solutions; D013696:Temperature; D014026:Nicotiana; D014407:Tumor Cells, Cultured
D012906:Smoke; D012996:Solutions; D009538:Nicotine; D015230:Prostaglandin D2; D002118:Calcium