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Infection and Immunity, June 2007, p. 2699-2707, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01788-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Wild-Type and Interleukin-10-Deficient Regulatory T Cells Reduce Effector T-Cell-Mediated Gastroduodenitis in Rag2–/– Mice, but Only Wild-Type Regulatory T Cells Suppress Helicobacter pylori Gastritis{triangledown}

Chung-Wei Lee,1,2 Varada P. Rao,1 Arlin B. Rogers,1 Zhongming Ge,1 Susan E. Erdman,1 Mark T. Whary,1 and James G. Fox1,2*

Division of Comparative Medicine,1 Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts2

Received 9 November 2006/ Returned for modification 14 December 2006/ Accepted 22 February 2007

CD4+ CD45RBhi CD25– effector T cells (TE) promote Helicobacter pylori gastritis in mice, and CD4+ CD45RBlo CD25+ regulatory T cells (TR) are anti-inflammatory. Using adoptive transfer into H. pylori-infected Rag2–/– mice, we evaluated effects of wild-type (wt) C57BL/6 or congenic interleukin-10-deficient (IL-10–/–) TR cells on gastritis, gastric cytokines, and H. pylori colonization. Infected Rag2–/– mice colonized in the corpus and antrum with 105 to 106 H. pylori CFU/gram without associated gastritis. TE cell transfer caused morbidity and an H. pylori-independent pangastritis and duodenitis (gastroduodenitis) associated with increased expression of gamma interferon (IFN-{gamma}) and tumor necrosis factor alpha. TE cell transfer to H. pylori-infected mice led to additive corpus gastritis associated with inflammatory cytokine expression and reduced colonization. wt TR cells reduced morbidity, H. pylori corpus gastritis, gastroduodenitis, and inflammatory cytokine expression and reversed the decline in H. pylori colonization attributable to TE cells. Although less effective than wt TR cells, IL-10–/– TR cells also reduced morbidity and gastroduodenitis but did not reduce H. pylori corpus gastritis or impact TE cell inhibition of colonization. Gastric tissues from mice receiving wt TR cells expressed higher levels of Foxp3 compared to recipients of IL-10–/– TR cells, consistent with lower regulatory activity of IL-10–/– TR cells. These results demonstrate that wt TR cells suppressed TE-cell-mediated H. pylori-independent gastroduodenitis and H. pylori-dependent corpus gastritis more effectively than IL-10–/– TR cells. Compartmental differences in TE-cell- and H. pylori-mediated inflammation and in regulatory effects between wt TR and IL-10–/– TR cells suggest that IL-10 expression by wt TR cells is important to regulatory suppression of gastric inflammation.

* Corresponding author. Mailing address: Massachusetts Institute of Technology, 77 Massachusetts Ave., Cambridge, MA 02139. Phone: (617) 253-1735. Fax: (617) 258-5708. E-mail: jgfox{at}mit.edu

{triangledown} Published ahead of print on 12 March 2007.

Editor: A. D. O'Brien

Infection and Immunity, June 2007, p. 2699-2707, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01788-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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