Figure 1.

Diminished or enhanced intestinal PRR signals may promote intestinal inflammation and tumorigenesis. PRR signals are maintained at a critical threshold to maintain intestinal homeostasis. PRR signals may be required to restore barrier function after epithelial insult and for protective immunity against pathogens; impairment of these processes caused by insufficient PRR signaling may result in pathogen outgrowth and, indirectly, excessive subsequent inflammation (left). Excessive PRR-driven repair or inflammatory responses (right) may also threaten homeostasis, e.g., through dysregulated epithelial proliferation leading to tumorigenesis and overexuberant pathogenic inflammatory responses to the intestinal microbiota.