Send to

Choose Destination
Clin Immunol. 2002 Sep;104(3):274-81.

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

Author information

Department of Pathology, University of Iowa College of Medicine, Iowa City 52242, USA.


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.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center