ArticleCellular & molecular immunology2024
The chemerin-CMKLR1 axis in keratinocytes impairs innate host defense against cutaneous Staphylococcus aureus infection.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- CMKLR1 as a Therapeutic Target: Vitamin D-Mediated Suppression of Inflammation and Oxidative Stress in SA-AKI.Molecular biotechnology · 2026Article
- Decoding chemerin proteolytic processing and isoform signaling across disease contexts.iScience · 2026Review
- Targeting the CMKLR1-Mediated Signaling Rebalances Immunometabolism State in Middle-Age Testicular Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026Review
- Blepharitis driven by microbiome dysbiosis andFrontiers in medicine · 2026Review
- The Role of Selected Proteins in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2025Review
- Effect of adipokines on bone marrow mesenchymal stem cell function.World journal of stem cells · 2025Review
- Article
- A Cross-Sectional Study: Systematic Quantification of Chemerin in Human Cerebrospinal Fluid.Biomedicines · 2024Article
- Review
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
Abstract
The skin is the most common site of Staphylococcus aureus infection, which can lead to various diseases, including invasive and life-threatening infections, through evasion of host defense. However, little is known about the host factors that facilitate the innate immune evasion of S. aureus in the skin. Chemerin, which is abundantly expressed in the skin and can be activated by proteases derived from S. aureus, has both direct bacteria-killing activity and immunomodulatory effects via interactions with its receptor CMKLR1. Here, we demonstrate that a lack of the chemerin/CMKLR1 axis increases the neutrophil-mediated host defense against S. aureus in a mouse model of cutaneous infection, whereas chemerin overexpression, which mimics high levels of chemerin in obese individuals, exacerbates S. aureus cutaneous infection. Mechanistically, we identified keratinocytes that express CMKLR1 as the main target of chemerin to suppress S. aureus-induced IL-33 expression, leading to impaired skin neutrophilia and bacterial clearance. CMKLR1 signaling specifically inhibits IL-33 expression induced by cell wall components but not secreted proteins of S. aureus by inhibiting Akt activation in mouse keratinocytes. Thus, our study revealed that the immunomodulatory effect of the chemerin/CMKLR1 axis mediates innate immune evasion of S. aureus in vivo and likely increases susceptibility to S. aureus infection in obese individuals.
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