Share this article on:

Role of Eosinophils in Inflammatory Bowel and Gastrointestinal Diseases

Woodruff, Samantha A; Masterson, Joanne C; Fillon, Sophie; Robinson, Zachary D; Furuta, Glenn T

Journal of Pediatric Gastroenterology & Nutrition: June 2011 - Volume 52 - Issue 6 - p 650–661
doi: 10.1097/MPG.0b013e3182128512
Invited Review

Inflammatory bowel diseases (IBD) are characterized by the invasion of leukocytes into the intestinal mucosa. However, a mixed inflammatory picture is observed that includes neutrophils, lymphocytes, monocytes, and eosinophils. To this day, the role of eosinophils in health and in disease remains unclear. Investigations into their function stem primarily from allergic diseases, asthma, and parasitic infections. This makes it even more difficult to discern a role for the fascinating eosinophil in IBDs because, unlike the lung or the skin, eosinophils reside in normal intestinal mucosa and increase in disease states; consequently, an intricate system must regulate their migration and numbers. These granulocytes are equipped with the machinery to participate in gastrointestinal (GI) inflammation and in the susceptible microenvironment, they may initiate or perpetuate an inflammatory response. A significant body of literature characterizes eosinophils present in the GI microenvironment where they have the potential to interact with other resident cells, thus promoting intestinal remodeling, mucus production, epithelial barrier, cytokine production, angiogenesis, and neuropeptide release. A number of lines of evidence support both potential beneficial and deleterious roles of eosinophils in the gut. Although studies from the gut and other mucosal organs suggest eosinophils affect mucosal GI inflammation, definitive roles for eosinophils in IBDs await discovery.

Digestive Health Institute, Gastrointestinal Eosinophilic Diseases Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, The Children's Hospital, Denver, CO, USA.

Received 30 November, 2010

Accepted 26 January, 2011

Address correspondence and reprint requests to Glenn T. Furuta, 13123 East 16th Ave, B290, Aurora, CO 80045 (e-mail: furuta.glenn@tchden.org).

Samantha A. Woodruff and Joanne C. Masterson participated equally in this study.

The authors report no conflicts of interest.

Copyright 2011 by ESPGHAN and NASPGHAN