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 stimulation, and to study the relationships between its impairment, if any, and blood indices of the nutritional and inflammatory status in elderly 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 correlation we found between basal chemiluminescence and immunoglobulins levels, IgM, IgG and IgA in the whole EP sample, and IgG in the N-Inf group, suggests that it could be linked to the cytokine imbalance that favours 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 EP and unexpectedly was less marked in group Inf EP. This observation suggests a relative impairment in EP phagocytic adaptive responses to inflammatory conditions. This suggestion was confirmed by the absence of significant differences between the chemiluminescence index CLI calculated after phorbol myrisate acetate (PMA) stimulation in group Inf vs. N-Inf EP, and by the lower CLI observed in group Inf phagocytes stimulated by opsonized zymosan. The role of blood changes associated with inflammation and/or nutrition in this relative impairment is supported by the positive correlations that we observed between CLI and acute-phase proteins. The overproduction of OFR could be partially responsible for the tissue damage, lymphocyte function impairment and the increased lethality of infectious diseases characteristic of elderly patients. inflammatory disorders seem to be linked to a relative impairment of the phagocyte adaptive response.