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Dermal adipocytes protect against invasive Staphylococcus aureus skin infection
Open accessAbstract
Skin infection triggers fat responses: Obesity is associated with chronic inflammation, but does fat tissue offer protection during infection? Zhang et al. noticed that the fat layers in the skin of mice thickened after inoculation with the pathogenic bacterium Staphylococcus aureus (see the Perspective by Alcorn and Kolls). Mutant mice incapable of forming new fat cells were more susceptible to infection. The differentiating fat cells secreted a small-molecule peptide called cathelicidin, specifically in response to the infection. By contrast, mature fat cells produce less cathelicidin, and are thus less protective. Science , this issue p. 67 ; see also p. 26
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“During S. aureus subcutaneous infection in mice, dermal fibroblasts undergo reactive adipogenesis and expand as preadipocytes that secrete CAMP (Cathelicidin Antimicrobial Peptide) [97].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [97]
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“epicutaneous and intradermal infection elicits different immune responses [41, 42]”
From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [42]
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Metadata
- Authors
- Zhang, L.-J., Guerrero-Juarez, C. F., Hata, T., Bapat, S. P., Ramos, R., Plikus, M. V., & Gallo, R. L.
- Affiliations
- University of California San Diego (US)
- Department of Developmental and Cell Biology, Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, Irvine, CA 92697, USA.
- Salk Institute for Biological Studies (US)
- University of California, Irvine (US)
- Corresponding author
- Gallo, Richard L.
- Venue
- Science
- Published
- 2015-01-02
- Volume
- 347
- Issue
- 6217
- Pages
- 67-71
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4318537
- OpenAlex
- W2021691433
- Cited by
- 471
- References
- 38
- Citations by year
- 2026: 30 · 2025: 37 · 2024: 47 · 2023: 43 · 2022: 46 · 2021: 52 · 2020: 36 · 2019: 44 · 2018: 45 · 2017: 36 · 2016: 30 · 2015: 25
- FWCI
- 38.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- NIH (R01 AI083358, R01AI052453, AR052728, DK096828)
- California Institute for Regenerative Medicine (TG2-01152)
- The Atopic Dermatitis Research Network (HHSN272201000020C)
- Edward Mallinckrodt Jr. Foundation Research
- Dermatology Foundation Research
- NIH NIAMS (R01-AR067273)
- NIH MBRS-IMSD (GM055246)
- NSF Graduate Research Fellowship (DGE-1321846)
- Topics
- Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Keywords
- Staphylococcus aureus, skin infections, host defense, adipogenesis, preadipocyte proliferation, cathelicidin, antimicrobial peptides, PPARγ, Zfp423, bacterial virulence
- MeSH terms
- Animals, DNA-Binding Proteins, Mice, Mutant Strains, Staphylococcal Skin Infections, Staphylococcus aureus, Transcription Factors, Adipocytes, Dermis, Antimicrobial Cationic Peptides, 3T3-L1 Cells, Adipogenesis, Mice, Cathelicidins, Host-Pathogen Interactions
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