TRIF-Dependent Innate Immune Activation Is Critical for Survival to Neonatal Gram-Negative Sepsis | Zendy

Alex G. Cuenca | Zendy; Dallas N. Joiner | Zendy; Lori F. Gentile | Zendy; Ángela Cuenca | Zendy; James L. Wynn | Zendy; Kindra M. KellyScumpia | Zendy; Philip O. Scumpia | Zendy; K.E. Behrns | Zendy; Philip A. Efron | Zendy; Dina C. Nacionales | Zendy; Chao Lui | Zendy; Shan M. Wallet | Zendy; Westley H. Reeves | Zendy; Clayton E. Mathews | Zendy; Lyle L. Moldawer | Zendy

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TRIF-Dependent Innate Immune Activation Is Critical for Survival to Neonatal Gram-Negative Sepsis

Author(s) -

Alex G. Cuenca,

Dallas N. Joiner,

Lori F. Gentile,

Ángela Cuenca,

James L. Wynn,

Kindra M. KellyScumpia,

Philip O. Scumpia,

K.E. Behrns,

Philip A. Efron,

Dina C. Nacionales,

Chao Lui,

Shan M. Wallet,

Westley H. Reeves,

Clayton E. Mathews,

Lyle L. Moldawer

Publication year - 2014

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1302676

Subject(s) - trif , sepsis , bacteremia , innate immune system , neonatal sepsis , immunology , peritonitis , medicine , signal transducing adaptor protein , immune system , tlr4 , biology , toll like receptor , receptor , microbiology and biotechnology , antibiotics

Current evidence suggests that neonatal immunity is functionally distinct from adults. Although TLR signaling through the adaptor protein, MyD88, has been shown to be critical for survival to sepsis in adults, little is known about the role of MyD88 or TRIF in neonatal sepsis. We demonstrate that TRIF(-/-) but not MyD88(-/-) neonates are highly susceptible to Escherichia coli peritonitis and bacteremia. This was associated with decreased innate immune recruitment and function. Importantly, we found that the reverse was true in adults that MyD88(-/-) but not TRIF(-/-) or wild-type adults are susceptible to E. coli peritonitis and bacteremia. In addition, we demonstrate that TRIF but not MyD88 signaling is critical for the TLR4 protective adjuvant effect we have previously demonstrated. These data suggest a differential requirement for the survival of neonates versus adults to Gram-negative infection, and that modulation of TRIF in neonates can be used to augment survival to neonatal sepsis.

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