Interleukin-17 and -22 synergy linking inflammation and EMT-dependent fibrosis in Sjögren’s syndrome | doi.page

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Interleukin-17 and -22 synergy linking inflammation and EMT-dependent fibrosis in Sjögren’s syndrome

Clinical & Experimental Immunology2019Vol. 198(2), pp. 261–272

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Margherita Sisto, Loredana Lorusso, Roberto Tamma, Giuseppe Ingravallo, Doménico Ribatti, Sabrina Lisi

Abstract

Primary Sjögren's syndrome (pSS) is a chronic inflammatory, autoimmune and systemic disorder commonly associated with dry eyes and a dry mouth. Recently, the hypothetical link between epithelial-mesenchymal transition (EMT)-dependent salivary gland (SG) fibrosis and chronic inflammatory conditions has been suggested. In this study, we present data demonstrating a negative correlation of the epithelial marker E-cadherin expression and a positive correlation of mesenchymal vimentin and collagen type I expression with increasing degrees of tissue inflammation in pSS SG specimens. In addition, as it is not clear whether dysregulated cytokines in pSS, interleukin (IL)-17 and IL-22 may also contribute to the EMT-dependent fibrosis process, the effect of IL-17 and IL-22 treatment on EMT-dependent SG fibrosis was evaluated in primary human salivary gland epithelial cells (SGEC) isolated from healthy subjects. Here we present data demonstrating that IL-17 and IL-22 can induce SGEC to undergo a morphological and phenotypical transition to a mesenchymal phenotype. In support of this, vimentin and collagen type I were up-regulated while a decreased expression of E-cadherin occurs after interleukin treatment, and co-operation between IL-17 and Il-22 was required to induce the EMT.

Citations Over TimeTop 10% of 2019 papers

Abstract

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