AI Article Synopsis
- The study investigates the role of the Fas/FasL pathway in apoptosis and its connection to atopic dermatitis (AD) using mouse models.
- The mice used were wild-type and two strains deficient in Fas and FasL, and various assessments were made through staining and PCR to analyze inflammation and immune response.
- Findings indicated that mice lacking Fas and FasL showed worsened symptoms of AD, including increased skin thickness and inflammation, suggesting that Fas-mediated apoptosis helps control local inflammation and may influence AD development.
Article Abstract
Objective And Design: The aim of this study was to elucidate the role of apoptosis mediated through Fas/FasL pathway using the mouse model of atopic dermatitis (AD).
Materials And Treatment: AD was induced by epicutaneous application of ovalbumin (OVA) in wild-type C57BL/6, B6. MRL-Faslpr/J (Fas-) and B6Smn.C3-Faslgld/J (FasL-) mouse strains.
Methods: Skin samples were subjected to staining for Fas/FasL expression, M30 epitope and assessment of inflammatory response via immunohistochemical staining. Cytokine and chemokine production was assessed by real-time PCR.
Results: In comparison to wild-type mice, OVA sensitization of Fas- and FasL-deficient mice led to increased epidermal and dermal thickness, collagen deposition and local inflammation consisting of macrophages, neutrophils and CD4+ T cells. Fas- and FasL-deficient mice showed increased total counts of regulatory T cells (Tregs) and IgE levels in blood as well as increased expression of IL-1β, IL-4, IL-5, IL-13 and TGF-1β mRNA in comparison to wild-type mice. On the other hand, expression of CXCL9 and CXCL10, IL-17 mRNAs in the skin samples in Fas- and FasL-deficient mice was decreased.
Conclusions: Our results show that lack of the Fas-induced apoptosis leads to exacerbation of AD characteristics such as Th2 inflammation and dermal thickening. Therefore, Fas receptor can play an important role in AD pathogenesis by controlling development of the local inflammation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5501908 | PMC |
| http://dx.doi.org/10.1007/s00011-017-1049-z | DOI Listing |
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