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Reciprocal Interactions between Commensal Bacteria and Intraepithelial Lymphocytes during Mucosal Injury¹

Anisa S. Ismail, Cassie L. Behrendt and Lora V. Hooper^2,*,,

^* Howard Hughes Medical Institute, Department of Immunology, and Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390

The intestinal mucosal surface is in direct contact with a vast beneficial microbiota. The symbiotic nature of this relationship is threatened when the surface epithelium is injured, yet little is known about how mucosal surfaces maintain homeostasis with commensal microbes following damage. Intraepithelial lymphocytes ( IEL) reside at the gut epithelial surface, where they stimulate mucosal healing following acute injury. A genome-wide analysis of the IEL response to dextran sulfate sodium-induced colonic damage revealed induction of a complex transcriptional program, including coordinate regulation of cytoprotective, immunomodulatory, and antibacterial factors. Studies in germfree mice demonstrated that commensal microbiota regulate key components of this transcriptional program, thus revealing a dialogue between commensal bacteria and IEL in injured epithelia. Analysis of TCR-deficient mice indicated that T cells are essential for controlling mucosal penetration of commensal bacteria immediately following dextran sulfate sodium-induced damage, suggesting that a key function of IEL is to maintain host-microbial homeostasis following acute mucosal injury. Taken together, these findings disclose a reciprocal relationship between T cells and intestinal microbiota that promotes beneficial host-microbial relationships in the intestine.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grant DK070855, the Crohn’s and Colitis Foundation of America, and a Burroughs Wellcome Foundation New Investigators in the Pathogenesis of Infectious Diseases Award (to L.V.H.). A.S.I. was supported by National Institutes of Health Training Grant AI005284.

² Address correspondence and reprint requests to Dr. Lora V. Hooper, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390. E-mail address: lora.hooper{at}utsouthwestern.edu

³ Abbreviations used in this paper: IEL, intraepithelial lymphocyte; DSS, dextran sulfate sodium; KGF, keratinocyte growth factor; MLN, mesenteric lymph node; PAP, pancreatitis-associated protein; Q-PCR, quantitative real-time PCR.

⁴ The online version of this article contains supplemental material.

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The JI 2009 182: 2555-2556. [Full Text]