Respiratory Mucosal Immunity: Physiology and Implications in Critical Care Medicine

Abstract

Respiratory mucosa is the first-line defense against external threat, notably from microbial origin. Indeed, it is a physical barrier against pathogens invasion but it also has major immune functions. Epithelial cells have innate immunity receptors (pathogen recognition receptors), which allow them to detect molecular patterns presented by microorganisms. Activation of these receptors leads to an inflammatory response of variable intensity. Epithelial cells also have the ability to modulate and lessen the inflammatory response triggered. Regulation of inflammatory response of the respiratory mucosa is highly complex and implies numerous cellular and molecular effectors, but two cytokines, Interleukin (IL)-17 and IL-22, are noteworthy. Thus, respiratory epithelium acts as both a sensor and an effector of the immune response, and this double function can be deregulated under various pathologic conditions. Dysfunction of epithelial response can be induced by respiratory supportive treatments, notably mechanical ventilation. However, alterations of epithelial functions are principally described during inflammatory process, either acute (e.g., acute respiratory distress syndrome) or chronic (e.g., chronic obstructive pulmonary disease). Respiratory epithelium is a key player in the physical and functional restoration of respiratory mucosa and so developing the therapeutic strategies to protect epithelial integrity might help in preventing pathological amplification of local inflammation and/or limiting pathogens dissemination.