Purpose of review: Recent advances in molecular techniques have enabled a deep view into the structure and function of the host's immune system and the stably associated commensal intestinal flora. This review outlines selected aspects of the interplay of innate immune recognition and effectors that shape the ecological niches for the intestinal microbiota.
Recent findings: Several studies have demonstrated a pivotal role of innate immune receptor pathways (NOD-like receptors and Toll-like receptors) for the maintenance of microbial communities in the gut. Genetic deficiencies in these pathways have been associated with increased susceptibility to inflammation that in animal models can be transmitted via direct contact or by stool transplantation in the absence of abundant pathogens.
Summary: The genetic architecture of the human host shapes the diversity and function of its stably associated intestinal microflora. Innate immune receptors such as NOD2 or the inflammasome component NOD-like receptor, pyrin-domain containing 6 play a major role in licensing the microbiota under physiological conditions. Understanding the symbiotic interplay in the intestinal tract should help develop procedures and therapeutic interventions aiming at the identification and restoration of disturbed microbiota states. Indeed, these states may be the missing trigger factor for the manifestation of a multitude of civilization disorders including inflammatory bowel disease and gastrointestinal cancer.