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Interleukin‐31 induces cytokine and chemokine production from human bronchial epithelial cells through activation of mitogen‐activated protein kinase signalling pathways: implications for the allergic response

Interleukin‐31 (IL‐31) is a novel T‐helper‐lymphocyte‐derived cytokine that plays an important role in allergic skin inflammation and atopic dermatitis. It has recently been implicated in bronchial inflammation. We investigated the functions and mechanisms of IL‐31‐induced activation of human bronchial epithelial cells. The gene and protein expressions of candidate cytokines/chemokines from IL‐31‐stimulated human bronchial epithelial BEAS‐2B cells were first quantified by quantitative real‐time polymerase chain reaction and enzyme‐linked immunosorbent assay, respectively. The activity of different mitogen‐activated protein kinases (MAPKs) in IL‐31‐stimulated BEAS‐2B cells was assessed by Western blot. The IL‐31 could significantly elevate the gene and protein expressions of epidermal growth factor (EGF), vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein‐1 (MCP‐1/CCL2) of BEAS‐2B cells in both time‐dependently and dose‐dependently. Combination of IL‐31 with either IL‐4 or IL‐13 further enhanced VEGF and CCL2 production while IL‐31 could synergistically augment the release of EGF, VEGF, CCL2, IL‐6 and IL‐8 in cocultures of BEAS‐2B cells and eosinophils. In addition, IL‐31 could activate p38 MAPK, extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) of BEAS‐2B cells. Selective inhibitors of p38 MAPK (SB203580), ERK (PD98059), and JNK (SP600125) could differentially inhibit the production of EGF, VEGF and CCL2, thereby suggesting a role for MAPKs in IL‐31 functions. In conclusion, the activation of MAPKs can be crucial for IL‐31‐mediated activation of bronchial epithelial cells, thereby providing an immunological role for IL‐31 in bronchial inflammation, at least partly, via epithelial EGF, VEGF and CCL2 production.