Resistin-like Molecule α Provides Vitamin-A-Dependent Antimicrobial Protection in the Skin

Tamia A. Harris; Sureka Gattu; Daniel C. Propheter; Zheng Kuang; Shai Bel; Kelly A. Ruhn; Andrew L. Chara; Marshall Edwards; Chenlu Zhang; Jay Hyun Jo; Prithvi Raj; Christos C. Zouboulis; Heidi H. Kong; Julia A. Segre; Lora V. Hooper

doi:10.1016/j.chom.2019.04.004

Resistin-like Molecule α Provides Vitamin-A-Dependent Antimicrobial Protection in the Skin

Tamia A. Harris
, Sureka Gattu
, Daniel C. Propheter
, Zheng Kuang
, Shai Bel
, Kelly A. Ruhn
, Andrew L. Chara
, Marshall Edwards
, Chenlu Zhang
, Jay Hyun Jo
, Prithvi Raj
, Christos C. Zouboulis
, Heidi H. Kong
, Julia A. Segre
, Lora V. Hooper

University of Texas Southwestern Medical Center
National Institutes of Health
Brandenburg Medical School Theodor Fontane

Research output: Contribution to journal › Article › peer-review

81 Scopus citations

Abstract

Vitamin A regulates skin immunity via unknown mechanisms. Harris et al. show that RELMα is an antimicrobial protein expressed by epidermal cells that shapes resident skin bacterial communities and limits skin infection. RELMα is induced by dietary vitamin A and mediates vitamin-A-dependent resistance to skin infection.

Original language	English
Pages (from-to)	777-788.e8
Journal	Cell Host and Microbe
Volume	25
Issue number	6
DOIs	https://doi.org/10.1016/j.chom.2019.04.004
State	Published - 12 Jun 2019
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2019 Elsevier Inc.

Funding

We thank C.L. Behrendt-Boyd, T. Leal, and B. Hassell for their assistance with mouse experiments; S. Muhkerjee for her assistance with protein isolation and the liposome experiments; B. Chong for human skin samples; G. Lui for the staphyloxanthin-deficient Staphylococcus aureus strain; and T. Vandergriff for review of the skin histology. This work was supported by NIH grant R01 DK070855 (L.V.H.), a Burroughs Wellcome Foundation Investigators in the pathogenesis of Infectious Diseases Award (L.V.H.), a Welch Foundation (grant I-1874 to L.V.H.), the Walter M. and Helen D. Bader Center for Research on Arthritis and Autoimmune Diseases (L.V.H.), and the Howard Hughes Medical Institute (L.V.H.). S.G. was supported by NIH grant T32 AI007520 , D.C.P. was supported by NIH grants T32 AI007520 and F32 DK100074 , Z.K. was supported by NIH grant T32 AI005284 , and S.B. was supported by a Gruss-Lipper postdoctoral fellowship. J.-H.J. was supported by a grant from the Korean Health Technology R&D Project , Ministry of Health and Welfare , Republic of Korea ( HI15C1095 ) and the Intramural Research Program of the National Cancer Institute . H.H.K. was supported by the Intramural Research Programs of the National Cancer Institute, National Institute of Arthritis and Musculoskeletal and Skin Diseases . J.A.S was supported by the Intramural Research Programs of the National Human Genome Research Institute . T.A.H. was supported by a Dermatology Foundation Career Development Award, the UT Southwestern Disease Oriented Clinical Scholars Program, a Burroughs Wellcome Fund Career Award for Medical Scientists, and a Burroughs Wellcome Fund Postdoctoral Enrichment Program Award. We thank C.L. Behrendt-Boyd, T. Leal, and B. Hassell for their assistance with mouse experiments; S. Muhkerjee for her assistance with protein isolation and the liposome experiments; B. Chong for human skin samples; G. Lui for the staphyloxanthin-deficient Staphylococcus aureus strain; and T. Vandergriff for review of the skin histology. This work was supported by NIH grant R01 DK070855 (L.V.H.), a Burroughs Wellcome Foundation Investigators in the pathogenesis of Infectious Diseases Award (L.V.H.), a Welch Foundation (grant I-1874 to L.V.H.), the Walter M. and Helen D. Bader Center for Research on Arthritis and Autoimmune Diseases (L.V.H.), and the Howard Hughes Medical Institute (L.V.H.). S.G. was supported by NIH grant T32 AI007520, D.C.P. was supported by NIH grants T32 AI007520 and F32 DK100074, Z.K. was supported by NIH grant T32 AI005284, and S.B. was supported by a Gruss-Lipper postdoctoral fellowship. J.-H.J. was supported by a grant from the Korean Health Technology R&D Project, Ministry of Health and Welfare, Republic of Korea (HI15C1095) and the Intramural Research Program of the National Cancer Institute. H.H.K. was supported by the Intramural Research Programs of the National Cancer Institute, National Institute of Arthritis and Musculoskeletal and Skin Diseases. J.A.S was supported by the Intramural Research Programs of the National Human Genome Research Institute. T.A.H. was supported by a Dermatology Foundation Career Development Award, the UT Southwestern Disease Oriented Clinical Scholars Program, a Burroughs Wellcome Fund Career Award for Medical Scientists, and a Burroughs Wellcome Fund Postdoctoral Enrichment Program Award. T.A.H. designed and performed most experiments. S.G. performed experiments with SZ95 cell line in Figures 5A and 5B. C.C.Z. provided the SZ95 cells and revised the manuscript. D.C.P designed the expression constructs used in Figure 2 and performed the PI uptake assays. Z.K. performed statistical analysis of the transcriptomics data in Figures 1A, S1, and S6. S.B, A.C. K.A.R. and M.E. provided technical assistance with the mouse experiments in Figures 4 and 6. C.Z. assisted with RNA isolation and qRT-PCR analysis. J.-H.J, H.H.K, P.R. and J.A.S. performed DNA extraction and 16S rRNA analysis in Figures 3 and S5. T.A.H. and L.V.H. designed experiments, interpreted results, and wrote the manuscript. The authors declare no competing interests.

Funders	Funder number
UT Southwestern Disease Oriented Clinical Scholars Program
Walter M. and Helen D. Bader Center for Research on Arthritis and Autoimmune Diseases
National Institutes of Health	R01 DK070855
Howard Hughes Medical Institute	T32 AI005284, T32 AI007520, F32 DK100074
National Human Genome Research Institute
National Cancer Institute	ZIABC011558
National Institute of Arthritis and Musculoskeletal and Skin Diseases
Burroughs Wellcome Fund
Welch Foundation	I-1874
Dermatology Foundation
Ministry of Health and Welfare	HI15C1095
Norges Idrettshøgskole

Keywords

antimicrobial protein
bacteria
innate immunity
microbiome
skin
skin infection
vitamin A

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10.1016/j.chom.2019.04.004

Cite this

Harris, T. A., Gattu, S., Propheter, D. C., Kuang, Z., Bel, S., Ruhn, K. A., Chara, A. L., Edwards, M., Zhang, C., Jo, J. H., Raj, P., Zouboulis, C. C., Kong, H. H., Segre, J. A., & Hooper, L. V. (2019). Resistin-like Molecule α Provides Vitamin-A-Dependent Antimicrobial Protection in the Skin. Cell Host and Microbe, 25(6), 777-788.e8. https://doi.org/10.1016/j.chom.2019.04.004

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abstract = "Vitamin A regulates skin immunity via unknown mechanisms. Harris et al. show that RELMα is an antimicrobial protein expressed by epidermal cells that shapes resident skin bacterial communities and limits skin infection. RELMα is induced by dietary vitamin A and mediates vitamin-A-dependent resistance to skin infection.",

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AU - Chara, Andrew L.

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Resistin-like Molecule α Provides Vitamin-A-Dependent Antimicrobial Protection in the Skin

Abstract

Bibliographical note

Funding

Keywords

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