Notably, Tan et al., demonstrated that three chronic HDM experimental asthma mouse models, with distinct inflammatory profiles (eosinophilic, neutrophilic, and mixed granulocytic), all had decreased expression of claudin-5, -8, -18, and -23, ZO-1, and occludin, further suggesting that a dysfunctional epithelium is activating and maintaining inflammatory pathologies rather than inflammation as the initial source of epithelial wounding (Tan et al., 2019). This evidence concerns the gene TJP1 and asthma.