Ethanol inhibition of signal transduction in superoxide production by rat alveolar macrophages. A proposed mechanism for ethanol related pneumonia.
Alveolar macrophages and neutrophils produce superoxide and other free radicals which are important in killing bacteria. The focus of this paper is the inhibition by ethanol of superoxide production and anti-bacterial activity. The signal transduction pathways leading to superoxide production by phagocytic cells will be reviewed. Our hypothesis is that ethanol alters these signal transduction pathways. Stimulation of superoxide production can be initiated by concanavalin A and phorbol esters. Previously, there were reports by us that ethanol, in vitro, inhibits phorbol ester induced superoxide production in rat alveolar macrophages. Our present report states that concanavalin A induced superoxide production was more sensitive to ethanol inhibition than phorbol ester induced superoxide production. The ethanol induced inhibition of alveolar macrophage superoxide production provides a possible mechanism to explain the increased sensitivity of alcoholics to pneumonia.
Dorio
R J
RJ
Department of Pediatrics, Childrens Hospital, Los Angeles.
Forman
H J
HJ
D002450:Cell Communication / Q000187:drug effects*; D000431:Ethanol / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D010587:Phagocytosis / Q000187:drug effects; D011014:Pneumonia / Q000139:chemically induced* / Q000382:microbiology; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000378:metabolism*; D013481:Superoxides / Q000378:metabolism*
D013481:Superoxides; D000431:Ethanol