Disruption of the endopeptidase ADAM10-Notch signaling axis leads to skin dysbiosis and innate lymphoid cell-mediated hair follicle destruction

Hair follicles (HFs) function as hubs for stem cells, immune cells, and commensal microbes, which must be tightly regulated during homeostasis and transient inflammation. Here we found that transmembrane endopeptidase ADAM10 expression in upper HFs was crucial for regulating the skin microbiota and...

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Vydáno v:Immunity (Cambridge, Mass.) Ročník 54; číslo 10; s. 2321
Hlavní autoři: Sakamoto, Keiko, Jin, Seon-Pil, Goel, Shubham, Jo, Jay-Hyun, Voisin, Benjamin, Kim, Doyoung, Nadella, Vinod, Liang, Hai, Kobayashi, Tetsuro, Huang, Xin, Deming, Clay, Horiuchi, Keisuke, Segre, Julia A, Kong, Heidi H, Nagao, Keisuke
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 12.10.2021
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ISSN:1097-4180, 1097-4180
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Abstract Hair follicles (HFs) function as hubs for stem cells, immune cells, and commensal microbes, which must be tightly regulated during homeostasis and transient inflammation. Here we found that transmembrane endopeptidase ADAM10 expression in upper HFs was crucial for regulating the skin microbiota and protecting HFs and their stem cell niche from inflammatory destruction. Ablation of the ADAM10-Notch signaling axis impaired the innate epithelial barrier and enabled Corynebacterium species to predominate the microbiome. Dysbiosis triggered group 2 innate lymphoid cell-mediated inflammation in an interleukin-7 (IL-7) receptor-, S1P receptor 1-, and CCR6-dependent manner, leading to pyroptotic cell death of HFs and irreversible alopecia. Double-stranded RNA-induced ablation models indicated that the ADAM10-Notch signaling axis bolsters epithelial innate immunity by promoting β-defensin-6 expression downstream of type I interferon responses. Thus, ADAM10-Notch signaling axis-mediated regulation of host-microbial symbiosis crucially protects HFs from inflammatory destruction, which has implications for strategies to sustain tissue integrity during chronic inflammation.
AbstractList Hair follicles (HFs) function as hubs for stem cells, immune cells, and commensal microbes, which must be tightly regulated during homeostasis and transient inflammation. Here we found that transmembrane endopeptidase ADAM10 expression in upper HFs was crucial for regulating the skin microbiota and protecting HFs and their stem cell niche from inflammatory destruction. Ablation of the ADAM10-Notch signaling axis impaired the innate epithelial barrier and enabled Corynebacterium species to predominate the microbiome. Dysbiosis triggered group 2 innate lymphoid cell-mediated inflammation in an interleukin-7 (IL-7) receptor-, S1P receptor 1-, and CCR6-dependent manner, leading to pyroptotic cell death of HFs and irreversible alopecia. Double-stranded RNA-induced ablation models indicated that the ADAM10-Notch signaling axis bolsters epithelial innate immunity by promoting β-defensin-6 expression downstream of type I interferon responses. Thus, ADAM10-Notch signaling axis-mediated regulation of host-microbial symbiosis crucially protects HFs from inflammatory destruction, which has implications for strategies to sustain tissue integrity during chronic inflammation.Hair follicles (HFs) function as hubs for stem cells, immune cells, and commensal microbes, which must be tightly regulated during homeostasis and transient inflammation. Here we found that transmembrane endopeptidase ADAM10 expression in upper HFs was crucial for regulating the skin microbiota and protecting HFs and their stem cell niche from inflammatory destruction. Ablation of the ADAM10-Notch signaling axis impaired the innate epithelial barrier and enabled Corynebacterium species to predominate the microbiome. Dysbiosis triggered group 2 innate lymphoid cell-mediated inflammation in an interleukin-7 (IL-7) receptor-, S1P receptor 1-, and CCR6-dependent manner, leading to pyroptotic cell death of HFs and irreversible alopecia. Double-stranded RNA-induced ablation models indicated that the ADAM10-Notch signaling axis bolsters epithelial innate immunity by promoting β-defensin-6 expression downstream of type I interferon responses. Thus, ADAM10-Notch signaling axis-mediated regulation of host-microbial symbiosis crucially protects HFs from inflammatory destruction, which has implications for strategies to sustain tissue integrity during chronic inflammation.
Hair follicles (HFs) function as hubs for stem cells, immune cells, and commensal microbes, which must be tightly regulated during homeostasis and transient inflammation. Here we found that transmembrane endopeptidase ADAM10 expression in upper HFs was crucial for regulating the skin microbiota and protecting HFs and their stem cell niche from inflammatory destruction. Ablation of the ADAM10-Notch signaling axis impaired the innate epithelial barrier and enabled Corynebacterium species to predominate the microbiome. Dysbiosis triggered group 2 innate lymphoid cell-mediated inflammation in an interleukin-7 (IL-7) receptor-, S1P receptor 1-, and CCR6-dependent manner, leading to pyroptotic cell death of HFs and irreversible alopecia. Double-stranded RNA-induced ablation models indicated that the ADAM10-Notch signaling axis bolsters epithelial innate immunity by promoting β-defensin-6 expression downstream of type I interferon responses. Thus, ADAM10-Notch signaling axis-mediated regulation of host-microbial symbiosis crucially protects HFs from inflammatory destruction, which has implications for strategies to sustain tissue integrity during chronic inflammation.
Author Liang, Hai
Sakamoto, Keiko
Horiuchi, Keisuke
Jin, Seon-Pil
Voisin, Benjamin
Nadella, Vinod
Nagao, Keisuke
Kobayashi, Tetsuro
Huang, Xin
Jo, Jay-Hyun
Goel, Shubham
Deming, Clay
Segre, Julia A
Kong, Heidi H
Kim, Doyoung
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  surname: Sakamoto
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  organization: Cutaneous Leukocyte Biology Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Seon-Pil
  surname: Jin
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  organization: Cutaneous Leukocyte Biology Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Shubham
  surname: Goel
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  organization: Cutaneous Leukocyte Biology Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  surname: Kim
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  organization: Cutaneous Leukocyte Biology Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Vinod
  surname: Nadella
  fullname: Nadella, Vinod
  organization: Cutaneous Leukocyte Biology Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Hai
  surname: Liang
  fullname: Liang, Hai
  organization: Cutaneous Microbiome and Inflammation Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Tetsuro
  surname: Kobayashi
  fullname: Kobayashi, Tetsuro
  organization: Cutaneous Leukocyte Biology Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Xin
  surname: Huang
  fullname: Huang, Xin
  organization: Microbial Genomics Section, Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Clay
  surname: Deming
  fullname: Deming, Clay
  organization: Microbial Genomics Section, Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Keisuke
  surname: Horiuchi
  fullname: Horiuchi, Keisuke
  organization: Department of Orthopedic Surgery, National Defense Medical College, Saitama 359-8513, Japan
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  givenname: Julia A
  surname: Segre
  fullname: Segre, Julia A
  organization: Microbial Genomics Section, Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA
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  givenname: Heidi H
  surname: Kong
  fullname: Kong, Heidi H
  organization: Cutaneous Microbiome and Inflammation Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
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  fullname: Nagao, Keisuke
  email: keisuke.nagao@nih.gov
  organization: Cutaneous Leukocyte Biology Section, Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: keisuke.nagao@nih.gov
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Keywords pyroptosis
hair follicles
alopecia
Notch
ADAM10
skin microbiota
innate lymphoid cells
caspase
cicatricial alopecia
dysbiosis
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References 34635833 - Nat Rev Immunol. 2021 Nov;21(11):691. doi: 10.1038/s41577-021-00641-9.
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Snippet Hair follicles (HFs) function as hubs for stem cells, immune cells, and commensal microbes, which must be tightly regulated during homeostasis and transient...
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SubjectTerms ADAM10 Protein - immunology
Alopecia - immunology
Alopecia - pathology
Amyloid Precursor Protein Secretases - immunology
Animals
Corynebacterium
Dysbiosis - immunology
Dysbiosis - pathology
Female
Hair Follicle - immunology
Hair Follicle - pathology
Immunity, Innate
Inflammation - immunology
Inflammation - metabolism
Inflammation - pathology
Lymphocytes - immunology
Membrane Proteins - immunology
Mice
Receptors, Notch - immunology
Signal Transduction - immunology
Skin - immunology
Skin - microbiology
Skin - pathology
Title Disruption of the endopeptidase ADAM10-Notch signaling axis leads to skin dysbiosis and innate lymphoid cell-mediated hair follicle destruction
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