Journal
TISSUE BARRIERS
Volume 5, Issue 3, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21688370.2017.1341367
Keywords
epithelial barrier function; epithelial-mesenchymal transition; neutrophil; Oncostatin M; type 2 inflammation
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Funding
- NIH [R37HL068546, U19AI106683]
- Ernest S. Bazley Charitable Fund
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Mucosal epithelium maintains tissue homeostasis through many processes, including epithelial barrier function, which separates the environment from the tissue. The barrier hypothesis of type 2 inflammatory disease postulates that epithelial and epidermal barrier dysfunction, which cause inappropriate exposure to the environment, can result in allergic sensitization and development of type 2 inflammatory disease. The restoration of barrier dysfunction once it's lost, or the prevention of barrier dysfunction, have the potential to be exciting new therapeutic strategies for the treatment of type 2 inflammatory disease. Neutrophil-derived Oncostatin M has been shown to be a potent disrupter of epithelial barrier function through the induction of epithelial-mesenchymal transition (EMT). This review will discuss these events and outline several points along this axis at which therapeutic intervention could be beneficial for the treatment of type 2 inflammatory diseases.
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