Abstract
Atopic dermatitis (AD) is a common inflammatory skin disease. Staphylococcus aureus (S. aureus) colonization in skin lesions occurs in approximately 70% of AD patients. It has been found that IFN-λ1 can inhibit the colonization of S. aureus 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 S. aureus 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 S. aureus colonization in AD lesions. Our findings might have potential value in the treatment for AD.
Highlights
Atopic dermatitis is a common inflammatory skin disorder
To illustrate whether IFN-λ1 treatment could stimulate endogenous IFN-λ1 secretion, we studied the expression of IFN-λ1 and IL-28R (IL-28RA and IL-10 receptor B (IL-10RB)) by Quantitative real-time PCR (qPCR) and IL28RA by western blotting
Data are means ± SD. (n 3, *p < 0.05, **p < 0.01, ***p < 0.001 vs. keratinocyte culture medium (KCM) or KCM + siNC; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. SA or SA + siNC). It is well-established that IFN-λ represent an important frontline defense in barrier epithelia that fights against viral infections (Krug et al, 2020; Galani et al, 2021)
Summary
Atopic dermatitis is a common inflammatory skin disorder. AD is a type 2 inflammatory disease, with increased Th2 cytokine levels, such as interleukin (IL)-4, IL-5, and IL-13 (Eyerich and Novak, 2013). Increased Staphylococcus aureus skin colonization is another hallmark of AD, which is often associated with disease severity and exacerbation (Byrd et al, 2017; Tay et al, 2020). S. aureus was found in approximately 70% AD lesions and 39% non-lesional skin (Totte et al, 2016). It has been reported that S. aureus can impair barrier function, inhibit antimicrobial peptides (AMP) production, and promote viral loads of HSV-1 and Th2 response (Bin et al, 2012; Geoghegan et al, 2018).
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
