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Publication

Toxin-Triggered Interleukin-1 Receptor Signaling Enables Early-Life Discrimination of Pathogenic versus Commensal Skin Bacteria.

Cell host & microbe | 2019

The host must develop tolerance to commensal microbes and protective responses to infectious pathogens, yet the mechanisms enabling a privileged relationship with commensals remain largely unknown. Skin colonization by commensal Staphylococcus epidermidis facilitates immune tolerance preferentially in neonates via induction of antigen-specific regulatory T cells (Tregs). Here, we demonstrate that this tolerance is not indiscriminately extended to all bacteria encountered in this early window. Rather, neonatal colonization by Staphylococcus aureus minimally enriches for antigen-specific Tregs and does not prevent skin inflammation upon later-life exposure. S. aureus α-toxin contributes to this response by stimulating myeloid cell production of IL-1β, which limits S. aureus-specific Tregs. Loss of α-toxin or the IL-1 receptor increases Treg enrichment, whereas topical application of IL-1β or α-toxin diminishes tolerogenic responses to S. epidermidis. Thus, the preferential activation of a key alarmin pathway facilitates early discrimination of microbial "foe" from "friend," thereby preventing tolerance to a common skin pathogen.

Pubmed ID: 31784259 RIS Download

Research resources used in this publication

None found

Additional research tools detected in this publication

None found

Antibodies used in this publication

Associated grants

  • Agency: NIAID NIH HHS, United States
    Id: T32 AI060537
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK063720
  • Agency: NIAID NIH HHS, United States
    Id: T32 AI007334
  • Agency: NCI NIH HHS, United States
    Id: P30 CA082103
  • Agency: NIAID NIH HHS, United States
    Id: DP2 AI144968
  • Agency: NIGMS NIH HHS, United States
    Id: T32 GM008568
  • Agency: NIAMS NIH HHS, United States
    Id: K08 AR068409

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

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