| First Author | Serezani APM | Year | 2017 |
| Journal | J Allergy Clin Immunol | Volume | 139 |
| Issue | 1 | Pages | 142-151.e5 |
| PubMed ID | 27554818 | Mgi Jnum | J:314512 |
| Mgi Id | MGI:6819322 | Doi | 10.1016/j.jaci.2016.07.012 |
| Citation | Serezani APM, et al. (2017) IL-4 impairs wound healing potential in the skin by repressing fibronectin expression. J Allergy Clin Immunol 139(1):142-151.e5 |
| abstractText | BACKGROUND: Atopic dermatitis (AD) is characterized by intense pruritis and is a common childhood inflammatory disease. Many factors are known to affect AD development, including the pleiotropic cytokine IL-4. Yet little is known regarding the direct effects of IL-4 on keratinocyte function. OBJECTIVE AND METHODS: In this report RNA sequencing and functional assays were used to define the effect of the allergic environment on primary keratinocyte function and wound repair in mice. RESULTS: Acute or chronic stimulation by IL-4 modified expression of more than 1000 genes expressed in human keratinocytes that are involved in a broad spectrum of nonoverlapping functions. Among the IL-4-induced changes, repression of fibronectin critically impaired the human keratinocyte wound response. Moreover, in mouse models of spontaneous and induced AD-like lesions, there was delayed re-epithelialization. Importantly, topical treatment with fibronectin restored the epidermal repair response. CONCLUSION: Keratinocyte gene expression is critically shaped by IL-4, altering cell fate decisions, which are likely important for the clinical manifestations and pathology of allergic skin disease. |
