SCGB1A1 and chronic lung disease: Lung infection by viruses and bacteria are known to elicit greater inflammatory responses in the absence of SCGB1A1 (32–34), whereas respiratory distress decreases SCGB1A1 levels following acute lung injury (35); exposures to pollutants (36), cigarette smoke (37) and ozone (38); lung allograft rejection (39–41); respiratory infections (42, 43); and chronic lung diseases (44, 45).