Susceptibility to viral infections in chronic obstructive pulmonary disease:  role of epithelial cells.
OBJECTIVE
The aim is to understand how airway epithelial cells with compromised innate defense mechanisms enhance susceptibility to respiratory virus infections in chronic obstructive pulmonary disease (COPD).


RESULTS
Exacerbations associated with respiratory viruses are more severe and increase disease severity in COPD. Airway epithelial cells cultured from COPD patients show excessive innate immune response to viral infection and higher viral load compared with normal cells.


CONCLUSIONS
Airway epithelial cells are the first line of defense in the lung and are equipped with several lines of innate defense mechanisms to fight against invading pathogens including viruses. Under normal conditions, mucociliary and barrier functions of airway epithelial cells prevent virus binding and entry into the cells. Virus-infected airway epithelial cells also express various cytokines, which recruit and activate innate and adaptive immune cells ultimately controlling the infection and tissue damage. In COPD however, compromised mucociliary and barrier functions may increase virus binding and allow virus entry into airway epithelial cells. Virus-infected COPD airway epithelial cells also show disproportionate cytokine expression leading to inappropriate recruitment and activation of innate and adaptive immune cells. COPD airway epithelial cells also show defective antiviral responses. Such defects in innate defense mechanisms may increase susceptibility to viral infections and disease severity in COPD.
Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, Michigan 48109-5688, USA. usajjan@umich.edu
Uma S
US
Sajjan
D004198:Disease Susceptibility; D006801:Humans; D007113:Immunity, Innate; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications* / Q000276:immunology / Q000821:virology; D020545:Respiratory Mucosa / Q000276:immunology* / Q000821:virology; D012141:Respiratory Tract Infections / Q000276:immunology* / Q000821:virology; D014777:Virus Diseases / Q000276:immunology*