Research in the Evans lab focuses on how airway mucins regulate respiratory health and disease. Two secreted mucins--MUC5AC and MUC5B--are the predominant macromolecular components of airway mucus. MUC5AC and MUC5B regulate host mucosal defense in health, but their excessive or aberrant expression is associated with transient infections and with a wide range of lung diseases such as asthma, cystic fibrosis, chronic obstructive pulmonary disease, pulmonary fibrosis, and lung cancer.

Using genetic and respiratory challenge models, our group has pioneered efforts to determine the significance of Muc5ac and Muc5b in mouse lungs (‘MUC’ in humans, ‘Muc’ in mice). We have discovered critical beneficial roles for Muc5b in homeostasis and responses to infection. Conversely, we have identified required detrimental roles for Muc5ac in airflow obstruction and lung injury.

Current research programs involve investigating how these two mucins perform their specific functions. Efforts are underway to determine whether and how the effects of MUC5AC/Muc5ac and MUC5B/Muc5b are mediated intrinsically by their differential expression and structural heterogeneity. Additional projects focus on how Muc5ac and Muc5b interact with leukocytes and structural cells in the lungs to regulate tissue inflammation, injury, and repair.

These projects use of genetically engineered mice, including over-expressing, knockout, and gene-edited lines, to address how Muc5ac and Muc5b function singly and in combination. Projects include studies of the mucin proteins, their assembly, and their glycosylation.