The barrier hypothesis and Oncostatin M: Restoration of epithelial barrier function as a novel therapeutic strategy for the treatment of type 2 inflammatory disease

Kathryn L. Pothoven*, Robert P. Schleimer

*Corresponding author for this work

Research output: Contribution to journalReview article

11 Scopus citations

Abstract

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.

Original languageEnglish (US)
Article numbere1341367
JournalTissue Barriers
Volume5
Issue number3
DOIs
StatePublished - Jul 3 2017

Keywords

  • Oncostatin M
  • epithelial barrier function
  • epithelial-mesenchymal transition
  • neutrophil
  • type 2 inflammation

ASJC Scopus subject areas

  • Biochemistry
  • Histology
  • Cell Biology

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