Critical role of interferons in gastrointestinal injury repair

Constance McElrath, Vanessa Espinosa, Jian-Da Lin, Jianya Peng, Raghavendra Sridhar, Orchi Dutta, Hsiang-Chi Tseng, Sergey V. Smirnov, Heidi Risman, Marvin J. Sandoval, Viralkumar Davra, Yun-Juan Chang, Brian P. Pollack, Raymond B. Birge, Mark Galan, Amariliz Rivera, Joan E. Durbin and Sergei V. Kotenko ()
Additional contact information
Constance McElrath: Rutgers—The State University of New Jersey
Vanessa Espinosa: Rutgers—The State University of New Jersey
Jian-Da Lin: Rutgers—The State University of New Jersey
Jianya Peng: Rutgers—The State University of New Jersey
Raghavendra Sridhar: Rutgers—The State University of New Jersey
Orchi Dutta: Rutgers—The State University of New Jersey
Hsiang-Chi Tseng: Rutgers—The State University of New Jersey
Sergey V. Smirnov: Rutgers—The State University of New Jersey
Heidi Risman: Rutgers—The State University of New Jersey
Marvin J. Sandoval: New York University School of Medicine
Viralkumar Davra: Rutgers—The State University of New Jersey
Yun-Juan Chang: Rutgers—The State University of New Jersey
Brian P. Pollack: Atlanta Veterans Affairs Medical Center
Raymond B. Birge: Rutgers—The State University of New Jersey
Mark Galan: Rutgers—The State University of New Jersey
Amariliz Rivera: Rutgers—The State University of New Jersey
Joan E. Durbin: Rutgers—The State University of New Jersey
Sergei V. Kotenko: Rutgers—The State University of New Jersey

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract The etiology of ulcerative colitis is poorly understood and is likely to involve perturbation of the complex interactions between the mucosal immune system and the commensal bacteria of the gut, with cytokines acting as important cross-regulators. Here we use IFN receptor-deficient mice in a dextran sulfate sodium (DSS) model of acute intestinal injury to study the contributions of type I and III interferons (IFN) to the initiation, progression and resolution of acute colitis. We find that mice lacking both types of IFN receptors exhibit enhanced barrier destruction, extensive loss of goblet cells and diminished proliferation of epithelial cells in the colon following DSS-induced damage. Impaired mucosal healing in double IFN receptor-deficient mice is driven by decreased amphiregulin expression, which IFN signaling can up-regulate in either the epithelial or hematopoietic compartment. Together, these data underscore the pleiotropic functions of IFNs and demonstrate that these critical antiviral cytokines also support epithelial regeneration following acute colonic injury.

Date: 2021
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DOI: 10.1038/s41467-021-22928-0

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