This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Khan, W. I.
Right arrow Articles by Collins, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Khan, W. I.
Right arrow Articles by Collins, S. M.

 Previous Article  |  Next Article 

Infection and Immunity, May 2003, p. 2430-2438, Vol. 71, No. 5
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.5.2430-2438.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Modulation of Intestinal Muscle Contraction by Interleukin-9 (IL-9) or IL-9 Neutralization: Correlation with Worm Expulsion in Murine Nematode Infections

W. I. Khan,1 M. Richard,2 H. Akiho,1 P. A. Blennerhasset,1 N. E. Humphreys,3 R. K. Grencis,3 J. Van Snick,2 and S. M. Collins1*

Intestinal Disease Research Program, McMaster University, Hamilton, Ontario Canada,1 Ludwig Institute for Cancer Research, Brussels Branch and Christian de Duve Institute of Cellular Pathology, Université Catholique de Louvain, Brussels, Belgium,2 School of Biological Sciences, University of Manchester, Manchester, United Kingdom3

Received 22 August 2002/ Returned for modification 12 November 2002/ Accepted 4 February 2003

Immune responses associated with intestinal nematode infections are characterized by the activation of T-helper 2 (Th2) cells. Previous studies demonstrated that during Trichinella spiralis infection, Th2 cells contribute to the development of intestinal muscle hypercontractility and to worm eviction from the gut, in part through signal transducer and activator of transcription factor 6 (Stat6). Interleukin-9 (IL-9), a Th2-cell-derived cytokine, has pleiotropic activities on various cells that are not mediated through Stat6. In this study, we investigated the role of IL-9 in the generation of enteric muscle hypercontractility in mice infected with the intestinal parasite T. spiralis and the cecal parasite Trichuris muris. Treatment of mice with IL-9 enhanced infection-induced jejunal muscle hypercontractility and accelerated worm expulsion in T. spiralis infection. These effects were associated with an up-regulation of IL-4 and IL-13 production from in vitro-stimulated spleen cells. In addition, increases in the level of intestinal goblet cells and in the level of mouse mucosal mast cell protease 1 (MMCP-1) in serum were observed in infected mice following IL-9 administration. However, the neutralization of IL-9 by anti-IL-9 vaccination or by anti-IL-9 antibody had no significant effect on worm expulsion or muscle contraction in T. spiralis-infected mice. In contrast, the neutralization of IL-9 significantly attenuated T. muris infection-induced colonic muscle hypercontractility and inhibited worm expulsion. The attenuated expulsion of the parasite by IL-9 neutralization was not accompanied by changes in goblet cell hyperplasia or the MMCP-1 level. These findings suggest that IL-9 contributes to intestinal muscle function and to host protective immunity and that its importance and contribution may differ depending on the type of nematode infection.

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

Editor: J. M. Mansfield

Infection and Immunity, May 2003, p. 2430-2438, Vol. 71, No. 5
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.5.2430-2438.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wan, Y. Y., Flavell, R. A. (2009). How Diverse--CD4 Effector T Cells and their Functions. J Mol Cell Biol 1: 20-36 [Abstract] [Full Text]  
  • Steenwinckel, V., Louahed, J., Lemaire, M. M., Sommereyns, C., Warnier, G., McKenzie, A., Brombacher, F., Van Snick, J., Renauld, J.-C. (2009). IL-9 Promotes IL-13-Dependent Paneth Cell Hyperplasia and Up-Regulation of Innate Immunity Mediators in Intestinal Mucosa. J. Immunol. 182: 4737-4743 [Abstract] [Full Text]  
  • Motomura, Y, Ghia, J-E, Wang, H, Akiho, H, El-Sharkawy, R T, Collins, M, Wan, Y, McLaughlin, J T, Khan, W I (2008). Enterochromaffin cell and 5-hydroxytryptamine responses to the same infectious agent differ in Th1 and Th2 dominant environments. Gut 57: 475-481 [Abstract] [Full Text]  
  • Wang, H., Steeds, J., Motomura, Y., Deng, Y., Verma-Gandhu, M., El-Sharkawy, R. T, McLaughlin, J. T, Grencis, R. K, Khan, W. I (2007). CD4+ T cell-mediated immunological control of enterochromaffin cell hyperplasia and 5-hydroxytryptamine production in enteric infection. Gut 56: 949-957 [Abstract] [Full Text]  
  • GOODMAN, D., HAJI, H. J., BICKLE, Q. D., STOLTZFUS, R. J., TIELSCH, J. M., RAMSAN, M., SAVIOLI, L., ALBONICO, M. (2007). A COMPARISON OF METHODS FOR DETECTING THE EGGS OF ASCARIS, TRICHURIS, AND HOOKWORM IN INFANT STOOL, AND THE EPIDEMIOLOGY OF INFECTION IN ZANZIBARI INFANTS. Am J Trop Med Hyg 76: 725-731 [Abstract] [Full Text]  
  • Leech, M. D., Grencis, R. K. (2006). Induction of Enhanced Immunity to Intestinal Nematodes Using IL-9-Producing Dendritic Cells. J. Immunol. 176: 2505-2511 [Abstract] [Full Text]  
  • Khan, W. I., Motomura, Y., Blennerhassett, P. A., Kanbayashi, H., Varghese, A. K., El-Sharkawy, R. T., Gauldie, J., Collins, S. M. (2005). Disruption of CD40-CD40 ligand pathway inhibits the development of intestinal muscle hypercontractility and protective immunity in nematode infection. Am. J. Physiol. Gastrointest. Liver Physiol. 288: G15-G22 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»