Atopic dermatitis (AD) is a common inflammatory skin disease. () colonization in skin lesions occurs in approximately 70% of AD patients. It has been found that IFN-λ1 can inhibit the colonization of in normal human nasal mucosa. IFN-λ1 can increase IL-28RA in infected human keratinocytes. In this study, we found that IFN-λ1 can increase mRNA expression of FLG and antimicrobial peptides (AMPs) and inhibit TSLP mRNA expression in infected human keratinocytes. IFN-λ1 can increase intracellular ROS level, decrease STAT1 phosphorylation, and inhibit the colonization of in human primary keratinocytes. These effects were attenuated by knocking-down IL-28R and NADPH oxidase inhibitor, suggesting that this function was mediated by JAK-STAT1 signaling pathway. These results suggest that IFN-λ1 might have an inhibitory effect on colonization in AD lesions. Our findings might have potential value in the treatment for AD.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019897 | PMC |
http://dx.doi.org/10.3389/fphar.2021.652302 | DOI Listing |
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