Dietary alteration of the interaction between alveolar macrophages and lymphocytes in experimental tuberculosis

Due to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to digital@library.tamu.edu, referencing the URI of the item.Includes bibliographical references: p. 54-61.Issued also on microfiche from Lange Micrographics.To study the interaction of alveolar macrophages (AM) and splenocytes (SC) and the dietary effects on the interaction of AM and SC in a guinea pig model of pulmonary tuberculosis, the ConA-induced proliferation of SC was quantified under various conditions of co-culture with resident AM. Low numbers of AM did not inhibit proliferation, while high numbers of AM suppressed proliferation in the co-cultures. No nitrite could be detected in supernatant fluids of co-cultured AM and splenocytes. Attempts to stimulate guinea pig AM with LPS in combination with recombinant murine and human IFN-Y failed to generate nitric oxide metabolites. Live Listeria monoc3qogenes-activated guinea pig AM did not produce detectable nitrite. Supernatants from ConA-stimulated guinea pig SC and LPS did not induce AM to produce NO. The AM of a nonnally-nourished, high protein (HP) group inhiltited the proliferation of SC only at high concentrations. However, even at very low concentrations, the AM of malnourished, low protein (LP) guinea pigs inhibited the proliferation of splenocytes to ConA. Catalase and indomethacin did not reverse the inhibitory effects of either HP AM or LP AM. Non-inhibitory levels of AM infected with M. tuberculosis H37Rv enhanced the proliferation of SC to ConA. Infection with mycobacteria did not influence the proliferation of SC to ConA co-cultured with inhibitory levels of AM. Neither CD4 nor CD8 depletion changed the pattern of the interaction between AM and SC of normal or protein-deprived guinea pigs. These results suggest that resident alveolar macrophages regulate lymphocyte function in the guinea pig, but that NO is not one of the modulating factors. Cell contact is very important in the interaction of AM and SC. Dietary protein deficiency was associated with a 10-fold increase in suppressive activity by alveolar macrophages. Mycobacteria exert different effects on the interaction between AM and SC of HP and LP guinea pigs. The detrimental impact of chronic, moderate dietary protein deficiency on cellmediated immune responses and disease resistance in this guinea pig model of experimental pulmonary tuberculosis may be mediated by dietary effects on the interaction between AM and SC