Excessive airway mucus secretion plays an important role in the morbidity and pathogenesis of disorders characterized by airway inflammation, such as asthma, chronic bronchitis, and cystic fibrosis. Various mediators of immediate hypersensitivity and acute inflammation have been shown to increase secretion of mucin glycoproteins by human airway epithelial cells. Mucin glycoprotein products expressed by human airway epithelial cells are encoded for by at least four distinct genes. Pro-inflammatory cytokines, such as tumor necrosis factor ALPHA, interleukin- (IL) 1b, and IL-6 are each capable of inducing mucin hypersecretion from human airway organ cultures and primary cultures of human airway epithelial cells, as measured by enzyme-linked immunoabsorbent assay, using a monoclonal antibody that recognizes human airway mucins. Reverse transcription- polymerase chain reaction and ribonuclease protection assays have been developed to assess induction of mucin gene expression in response to pro-inflammatory and anti-inflammatory cytokines. One study has been published, and two others have been completed. Continuing studies will allow for better understanding of the role of individual mucin genes in cytokine-mediated airway inflammatory events, as well as the intracellular events associated with changes in airway mucin gene expression. An improved understanding of the role of inflammatory cytokines in the induction of airway mucin hypersecretion may further our understanding of the pathophysiology of disorders characterized by airway inflammation.
