A role of Toll-IL-1 receptor domain-containing adaptor-inducing IFN-β in the host response to Pseudomonas aeruginosa lung infection in mice

Melanie R. Power, Bo Li, Masahiro Yamamoto, Shizuo Akira, Tong Jun Lin

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

62 Citas (Scopus)

Resumen

Toll-IL-1R domain-containing adaptor-inducing IFN-β (TRIF) is an adaptor moiecnle that mediates a distinct TLR signaling pathway. Roles of TRIF in the host defense have been primarily associated with virus infections owing to the induction of IFN-αβ. In this study, we investigated a role of TRIF in Pseudomonas aeruginosa infection. In vitro, TRIF-deficient mouse alveolar and peritoneal macrophages showed a complete inhibition of RANTES (CCL5) production, severely impaired TNF and KC (CXCL1) production, and reduced NF-κB activation in response to P. aeruginosa stimulation. In vivo, TRIF-deficient mice showed a complete inhibition of RANTES production, a severely impaired TNF and KC production, and an efficient MIP-2 and IL-1β production in the lung following P. aeruginosa infection. This outcome was associated with a delayed recruitment of neutrophils into the airways. These results suggest that TRIF mediates a distinct cytokine/chemokine profile in response to P. aeruginosa infection. P. aeruginosa-induced RANTES prodection is completely dependent on TRIF pathway in mice. Importantly, TRIF deficiency leads to impaired clearance of P. aeruginosa from the long during the initial 24-48 h of infection. Thus, TRIF represents a novel mechanism involved in the development of host response to P. aeruginosa infection.

Idioma originalEnglish
Páginas (desde-hasta)3170-3176
Número de páginas7
PublicaciónJournal of Immunology
Volumen178
N.º5
DOI
EstadoPublished - mar. 1 2007

ASJC Scopus Subject Areas

  • Immunology and Allergy
  • Immunology

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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