Host–microbe interactions in the small bowelDavies, Julie M.; Abreu, Maria T.Current Opinion in Gastroenterology: March 2015 - Volume 31 - Issue 2 - p 118–123 doi: 10.1097/MOG.0000000000000143 SMALL INTESTINE: Edited by Fergus Shanahan Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The intestine – home to a vast microbiome – balances its immune reactivity on a knife's edge. This review will summarize recent studies examining innate immune signals that shape the microbiota, and how pathogens can usurp protective responses to their advantage. Recent findings Innate signaling uses several pathways to maintain epithelial defense. Toll-like receptor signaling through myeloid differentiation factor 88 maintains segregation between bacteria and the epithelium through production of antimicrobial proteins, and inflammasome signaling mediates efficient goblet cell release of mucus containing granules. Conversely, negative regulators of Toll-like receptor signaling help maintain a healthy microbiota resistant to pathogen infection. Methods to evade immune elimination by pathogens associated with human infections and inflammatory bowel disease are described. Emerging evidence that pattern recognition receptors can differentiate between commensals and pathogens will be examined. Summary The balance of innate signaling in the intestine is crucial to homeostasis: too little and bacteria can directly contact the epithelium, too much depletes the protective microbiota, creating a niche for pathogens. Understanding the dynamic interaction between the immune system and the microbiota in a variety of infection and inflammation models will hopefully translate to new therapies. Division of Gastroenterology, Department of Medicine, University of Miami, Miller School of Medicine, Miami, Florida, USA Correspondence to Maria T. Abreu, MD, Division of Gastroenterology, Department of Medicine, University of Miami, Miller School of Medicine, Miami, FL 33136, USA. Tel: +1 305 243 6404; fax: +1 305 243 6125; e-mail: firstname.lastname@example.org Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.