Role of MUC1 Mucin During the Respiratory Track Infection and Inflammation

K. Chul Kim
2010 Nihon Bika Gakkai Kaishi (Japanese Journal of Rhinology)  
Airway mucins are high molecular weight glycoproteins that are thought to play an important defensive role against inhaled pathogens. Twenty mucin genes MUC in human and Muc in nonhuman species have been cloned, ten of which are expressed in the respiratory track RT . Why so many mucins are expressed in the RT, however, remains unknown. To date, the only mucin gene product whose function is known in the RT is MUC1 which has been shown to play an important counter regulatory role during airway
more » ... flammation. While inflammation is an essential host defense mechanism against invading pathogens, the inflammatory response needs to be controlled once pathogens are cleared to avoid unnecessary damage to the host. MUC1 appears to mediate one of the mechanisms through which airway inflammation is controlled. Kim and Lillehoj, Am J Respir Cell Mol Biol 39 : 644, 2008 . In this lecture, I will focus on the role of MUC1 mucin in the context of airway inflammation. MUC1 is expressed on the surface of mucosal epithelial cells as well as hematopoietic cells. The anti inflammatory role of MUC1 is best illustrated using an airway Pseudomonas aeruginosa PA infection model. Briefly, PA entering the airway is recognized by various TLRs on the epithelial cells which results in the release of inflammatory mediators such as IL 8 and TNF α which, in turn, recruit neutrophils inducing airway inflammation. Inflammatory products such as neutrophil elastase and TNF α increase the levels of epithelial MUC1 thereby suppressing TLR signaling and ending the ongoing inflammatory response. Failure to upregulate MUC1 may result in a continuous influx of neutrophils into airways leading to injuries and remodeling of the airways, a major phenotype seen in COPD. MUC1 mucin seems to play a key role at the later stages of inflammation to prevent host damage through both the timely appearance and highly efficient intervention of the inflammatory mechanism.
doi:10.7248/jjrhi.49.83 fatcat:oleq4epo55bahgoytl4uh4lq6e