FUNCTION OF THE OXIDATIVE-METABOLISM OF PHAGOCYTES IN ELDERLY PEOPLE - RELATIONSHIP TO NUTRITIONAL AND INFLAMMATORY STATUS

The purpose of this study was to investigate the phagocyte production of oxygen-free radicals (OFR) in the whole blood of elderly patients ( EP), by measuring chemiluminescence at the basal state and after stimu lation, and to study the relationships between its impairment, if any, and blood indices of the nutritional and inflammatory status in elder ly patients with (Inf) and without (N-Inf) inflammatory diseases. The results showed that OFR production by resting circulating phagocytes, assessed by chemiluminescence on whole blood, is markedly increased in EP, irrespective of any in vitro stimulation. The significant correla tion we found between basal chemiluminescence and immunoglobulins leve ls, IgM, IgG and IgA in the whole EP sample, and IgG in the N-Inf grou p, suggests that it could be linked to the cytokine imbalance that fav ours Th2- and impairs Th1-type of cytokine production by T-cells in EP . The basal overproduction of OFR was observed both in Inf and N-Inf E P and unexpectedly was less marked in group Inf EP. This observation s uggests a relative impairment in EP phagocytic adaptive responses to i nflammatory conditions. This suggestion was confirmed by the absence o f significant differences between the chemiluminescence index CLI calc ulated after phorbol myrisate acetate (PMA) stimulation in group Inf v s. N-Inf EP, and by the lower CLI observed in group Inf phagocytes sti mulated by opsonized zymosan. The role of blood changes associated wit h inflammation and/or nutrition in this relative impairment is support ed by the positive correlations that we observed between CLI and acute -phase proteins. The overproduction of OFR could be partially responsi ble for the tissue damage, lymphocyte function impairment and the incr eased lethality of infectious diseases characteristic of elderly patie nts. inflammatory disorders seem to be linked to a relative impairment of the phagocyte adaptive response.