SUMMARY Resident microbes in skin and gut predominantly impact local immune cell function during homeostasis. However, colitis-associated neutrophilic skin disorders suggest possible breakdown of this compartmentalization with disease. Using a model wherein neonatal skin colonization by Staphylococcus epidermidis facilitates generation of commensal-specific tolerance and CD4+ regulatory T cells (Tregs), we ask whether this response is perturbed by gut inflammation. Chemically induced colitis is accompanied by intestinal expansion of S. epidermidis and reduces gut-draining lymph node (dLN) commensal-specific Tregs. It also results in reduced commensal-specific Tregs in skin and skin-dLNs and increased skin neutrophils. Increased CD4+ circulation between gut and skin dLN suggests that the altered cutaneous response is initiated in the colon, and resistance to colitis-induced effects in Cd4creIl1r1fl/fl mice implicate interleukin (IL)-1 in mediating the altered commensal-specific response. These findings provide mechanistic insight into observed connections between inflammatory skin and intestinal diseases.
Intestinal inflammation alters the antigen-specific immune response to a skin commensal
G. Merana,Laura R. Dwyer,M. Dhariwala,Antonin Weckel,Jeanmarie R. Gonzalez,Joy Okoro,Jarish N. Cohen,C. Tamaki,Jungmin Han,P. Tasoff,Yasmin Palacios-Calderon,C. Ha,S. Lynch,J. Segre,H. Kong,Michael G. Kattah,A. Ma,T. Scharschmidt
Published 2022 in Cell Reports
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PUBLICATION RECORD
- Publication year
2022
- Venue
Cell Reports
- Publication date
2022-05-01
- Fields of study
Biology, Medicine, Environmental Science
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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