Staphylococcus aureus Epicutaneous Exposure Drives Skin Inflammation via IL-36-Mediated T Cell Responses
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Staphylococcus aureus colonization contributes to skin inflammation in diseases such as atopic dermatitis, but the signaling pathways involved are unclear. Herein, epicutaneous S. aureus exposure to mouse skin promoted MyD88-dependent skin inflammation initiated by IL-36, but not IL-1α/β, IL-18, or IL-33. By contrast, an intradermal S. aureus challenge promoted MyD88-dependent host defense initiated by IL-1β rather than IL-36, suggesting that different IL-1 cytokines trigger MyD88 signaling depending on the anatomical depth of S. aureus cutaneous exposure. The bacterial virulence factor PSMα, but not α-toxin or δ-toxin, contributed to the skin inflammation, which was driven by IL-17-producing γδ and CD4+ T cells via direct IL-36R signaling in the T cells. Finally, adoptive transfer of IL-36R-expressing T cells to IL-36R-deficient mice was sufficient for mediating S. aureus-induced skin inflammation. Together, this study defines a previously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammation involving IL-36R/MyD88-dependent IL-17 T cell responses.
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In a mouse model, colonization with Staphylococcus aureus induces IL-36R- and IL-1R-dependent inflammation.
“Interestingly, in a mouse model, colonization with S. aureus induces IL-36R- and IL-1R-dependent inflammation73.”
From Atopic dermatitis: an expanding therapeutic pipeline for a complex disease (2022) · cites this paper as [73]
In the Results section on IL-36R signaling (page unavailable), mice lacking IL-36R had substantially less skin inflammation after epicutaneous S. aureus exposure, supporting IL-36R dependence. The IL-1R-dependent part is not supported: mice lacking either IL-1α or IL-1β had inflammation measures similar to controls, and the paper distinguishes this epicutaneous response from the IL-1β response to intradermal infection. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThere is increasing evidence that the IL-23-IL-17 axis and IL-36 may have a role in some AD subtypes, such as the intrinsic form and in Asian patients.
“there is increasing evidence that the IL-23–IL-17 axis as well as IL-36 (see above) may have a role, at least in some AD subtypes such as the so-called intrinsic form and in Asian patients73,103,117,123–125.”
From Atopic dermatitis: an expanding therapeutic pipeline for a complex disease (2022) · cites this paper as [73]
The Discussion (page unavailable) links IL-36 signaling to IL-17-producing T-cell responses in a mouse model of S. aureus-induced skin inflammation and relates the findings to human atopic dermatitis. It does not establish a role for the IL-23–IL-17 axis or address intrinsic atopic dermatitis or Asian patients, so the subtype-specific claim is not supported by this paper. (LLM, conf=0.86)
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- Authors
- Liu, H., Archer, N. K., Dillen, C. A., Wang, Y., Ashbaugh, A. G., Ortines, R. V., Kao, T., Lee, S. K., Cai, S. S., Miller, R. J., Marchitto, M. C., Zhang, E., Riggins, D. P., Plaut, R. D., Stibitz, S., Geha, R. S., & Miller, L. S.
- Affiliations
- Johns Hopkins University (US)
- Center for Biologics Evaluation and Research (US)
- Boston Children's Hospital (US)
- Corresponding author
- Miller, Lloyd S.
- ORCID
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2017-11
- Volume
- 22
- Issue
- 5
- Pages
- 653-666.e5
- ISSN
- 1931-3128 (ISSN-L)
- PMC
- PMC5774218
- OpenAlex
- W2767217104
- Cited by
- 263
- References
- 64
- Citations by year
- 2026: 26 · 2025: 27 · 2024: 41 · 2023: 33 · 2022: 30 · 2021: 29 · 2020: 27 · 2019: 31 · 2018: 16 · 2017: 3
- FWCI
- 23.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Host & Microbe (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (UM2AI117870)
- NIH (R01AR069502)
- Pfizer (WI214880)
- Topics
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Keywords
- Staphylococcus aureus, skin inflammation, IL-36, IL-36 receptor, MyD88 signaling, IL-17, γδ T cells, CD4+ T cells, staphylococcal virulence factors, atopic dermatitis, IL-1β, intradermal challenge, adoptive transfer
- MeSH terms
- Interleukin-33, Animals, Bacterial Toxins, Dermatitis, Atopic, Disease Models, Animal, Female, Hemolysin Proteins, Host-Parasite Interactions, Inflammation, Interleukin-1, Male, Mice, Inbred BALB C, Skin, Staphylococcal Infections, Staphylococcus aureus, T-Lymphocytes, CD4-Positive T-Lymphocytes, Cytokines, Receptors, Interleukin-1, Interleukin-17, Interleukin-18, Virulence Factors, Mice, Interleukin-1alpha, Interleukin-1beta, Myeloid Differentiation Factor 88
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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