Cytokines other than IL-4 and IL-13 may be responsible for increases in pendrin expression; IL-1β, a macrophage-secreted cytokine involved in the immunopathogenesis of asthma and COPD, has also been shown to increase pendrin levels in rodent and human bronchial epithelial cells [74, 90]. This evidence concerns the gene SLC26A4 and chronic obstructive pulmonary disease.