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 articlepeer-review

16 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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