The gastrointestinal tract in humans and animals contains a very large number of highly diverse microorganisms. This microbiota plays a major role in the host’s physiology, homeostasis, and well-being. It forms a barrier against infection, helps to develop and mature the immune system, and participates in the extraction of nutrients and energy from food. Various members of microbial community maintain the integrity of the intestinal barrier and promote epithelial repair after injury. The intestinal barrier defenses consist of the mucous layer, antimicrobial peptides, secretory IgA, and the epithelial barrier function by junctional adhesion complex. A healthy host exists in a state of balance with its microorganisms. A disruption of the microbial community increases the host’s susceptibility to infection. Although the immune response is necessary for the host to eliminate the invading pathogen, certain aspects of the host’s response may work to the pathogen’s advantage. Certain components of the microbiota have been shown to drive inflammatory response, which, if uncontrolled, has the potential to induce a pathological response, whereas others enhance or promote antiinflammatory responses. The effector microbial molecules are usually detected via receptor-signaling pathways including Toll-like receptors, NOD-like receptors, and C-type lectin receptors. These pattern-recognition receptors (PRRs) interact with and identify microbe-associated molecular patterns (MAMPs) of both commensal and pathogenic bacteria. PRRs signaling, once thought to exclusively yield pro-inflammatory activation by pathogenic bacteria, is now known to be differentially activated by commensal and probiotic bacteria to induce pathways involved in gut homeostasis, cytoprotection, epithelial cell proliferation, regulation of tight junctions, and antimicrobial peptide secretion. The microbial-epithelial cross-talk is fundamental in appreciating how the developing intestine achieves tolerance to bacteria and how dysregulation of this process may predispose the gut to inflammation and disease.
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