%0 Journal Article
%T The barrier hypothesis and Oncostatin M: Restoration of epithelial barrier function as a novel therapeutic strategy for the treatment of type 2 inflammatory disease
%A Kathryn L. Pothoven
%A Robert P. Schleimer
%J Archive of "Tissue Barriers".
%D 2017
%R 10.1080/21688370.2017.1341367
%X 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
%K epithelial barrier function
%K epithelial-mesenchymal transition
%K neutrophil
%K Oncostatin M
%K type 2 inflammation
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5571776/