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Infection and Immunity, February 2001, p. 838-844, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.838-844.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Critical Role for Signal Transducer and Activator of Transcription Factor 6 in Mediating Intestinal Muscle Hypercontractility and Worm Expulsion in Trichinella spiralis-Infected Mice

W. I. Khan,1 B. A. Vallance,1 P. A. Blennerhassett,1 Y. Deng,1 E. F. Verdu,1 K. I. Matthaei,2 and S. M. Collins1,*

Intestinal Disease Research Program, McMaster University, Hamilton, Ontario, Canada,1 and John Curtin School of Medical Research, Australian National University, Canberra, Australia2

Received 24 April 2000/Returned for modification 14 June 2000/Accepted 2 November 2000

Intestinal nematode infections in rats or mice are accompanied by intestinal muscle hyper contractility that may contribute to parasite expulsion from the gut. Previous studies demonstrated that both the expulsion of nematode parasites and the associated muscle hyper contractility are dependent on CD4+ T helper cells. Nevertheless, the precise immunological mechanism underlying changes in intestinal muscle function remains to be determined. In this study, we investigated the role of interleukin 4 (IL-4) and signal transducer and activator of transcription factor 6 (STAT6) in the development of intestinal muscle hypercontractility and worm expulsion by infecting IL-4 and STAT6-deficient mice with Trichinella spiralis. Worm expulsion was almost normal in IL-4-deficient mice but substantially delayed in STAT6-deficient mice. Consistent with delayed worm expulsion, we also observed a marked attenuation of carbachol-induced muscle contraction in STAT6-deficient mice but only a moderate decrease in muscle hypercontractility in IL-4-deficient mice. In addition, we also observed severe impairment of T helper type 2 cytokine responses and intestinal mucosal mastocytosis in STAT6-deficient mice, although some degree of intestinal tissue eosinophilia was evident in these animals. These results are consistent with the hypothesis that STAT6-dependent changes in intestinal muscle function contribute to host protection in nematode infection.

* Corresponding author. Mailing address: Room 4W8, HSC, McMaster University Medical Center, Hamilton, Ontario L8N 3Z5, Canada. Phone: (905) 521-2100, ext. 5255. Fax: (905) 521-4958. E-mail: scollins{at}fhs.csu.mcmaster.ca.

Infection and Immunity, February 2001, p. 838-844, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.838-844.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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