ALCOHOL-INDUCED INHIBITION OF ALVEOLAR MACROPHAGE OXIDANT RELEASE INVIVO AND INVITRO

Alcohol consumption is known to predispose the host to more frequent a nd severe bacterial infections, suggesting that alcohol compromises th e normal immune function of the lung. The pulmonary alveolar macrophag e is the resident host defense cell in the lung and forms the first li ne of defense against invading microorganisms. One of the mechanisms w hereby alveolar macrophages kill bacteria is by releasing toxic oxygen radical species, such as superoxide anion and hydrogen peroxide. We h ypothesized that chronic alcohol consumption caused alveolar macrophag e dysfunction leading to inhibition of oxidant production when stimula ted. Our data demonstrate that alveolar macrophages harvested from alc ohol-treated rats release significantly lower quantity (p < 0.05) of b oth superoxide anion and hydrogen peroxide when stimulated with severa l different types of stimuli including heat-killed Staphylococcus aure us, soluble immune complexes or phorbol myristate acetate. Pair-fed co ntrol rats who received isocaloric quantities of maltose dextrin in th eir diet to compensate for the alcohol were able to produce oxidants i n equal quantities when stimulated, to rats who were fed a normal diet . Similar results were noted in vitro experiments when alveolar macrop hages harvested from normal rats were incubated in vitro in alcohol-co ntaining media and then stimulated with the aforementioned stimuli. Al veolar macrophages, which had been incubated in alcohol for 4 hr, show ed significant decreases in their ability to produce superoxide anion. This defect was noticeable for a period up to 8 hr following removal of alveolar macrophages from the alcohol-containing media. The inabili ty of alveolar macrophages to release oxidants may cause a significant break in their bacteriocidal capacity leading to the establishment of overt pulmonary parenchymal infection.