Established T(H1) granulomatous responses induced by active Mycobacterium avium infection switch to T(H2) following challenge with Schistosoma mansoni.

Mycobacterium avium established a systemic infection with granulomatous inflammation in mice. Mice chronically infected with M. avium and subsequently co-infected with Schistosoma mansoni developed additional, but morphologically distinct, hepatic granulomas. Schistosome eggs were not deposited in the spleen, and splenic granulomas in co-infected mice contained mycobacteria. In complete contrast to the T(H1) cytokine pattern observed with granuloma lymphocytes from M. avium-infected mice, granuloma lymphocytes from co-infected mice stimulated with PPD elaborated IL-4, but not IFN-gamma. Furthermore, mycobacterial granulomas in concurrently infected mice contained large numbers of eosinophils, a feature never seen in granulomas of M. avium-infected mice. Serum IgG1 and IgE levels in concurrently infected mice were significantly higher, but IgG2a levels significantly lower, than those in M. avium-infected mice, further evidence that the T(H1) component induced by M. avium is modulated subsequent to co-infection with S. mansoni. The dominance of the T(H2) response observed in this model could have clinical implications in areas where parasites and mycobacteria co-exist.