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Infection induced inflammation impairs wound healing through IL-1ß signaling.
Shen, Simone; Miskolci, Veronika; Dewey, Colin N; Sauer, John-Demian; Huttenlocher, Anna.
Afiliação
  • Shen S; Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI, USA.
  • Miskolci V; Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI, USA.
  • Dewey CN; Department of Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, WI, USA.
  • Sauer JD; Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI, USA.
  • Huttenlocher A; Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI, USA.
iScience ; 27(4): 109532, 2024 Apr 19.
Article em En | MEDLINE | ID: mdl-38577110
ABSTRACT
Wound healing is impaired by infection; however, how microbe-induced inflammation modulates tissue repair remains unclear. We took advantage of the optical transparency of zebrafish and a genetically tractable microbe, Listeria monocytogenes, to probe the role of infection and inflammation in wound healing. Infection with bacteria engineered to activate the inflammasome, Lm-Pyro, induced persistent inflammation and impaired healing despite low bacterial burden. Inflammatory infections induced il1b expression and blocking IL-1R signaling partially rescued wound healing in the presence of persistent infection. We found a critical window of microbial clearance necessary to limit persistent inflammation and enable efficient wound repair. Taken together, our findings suggest that the dynamics of microbe-induced tissue inflammation impacts repair in complex tissue damage independent of bacterial load, with a critical early window for efficient tissue repair.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: IScience Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: IScience Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos
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