Host-microbe interactions in the small bowel

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.

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.

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.