Adenoviral Infection Decreases Mortality from Lipopolysaccharide-Induced Liver Failure Via Induction of TNF-α Tolerance | Zendy

Timur O. Yarovinsky | Zendy; Linda S. Powers | Zendy; Noah S. Butler | Zendy; Mary A. Bradford | Zendy; Martha M. Monick | Zendy; Gary W. Hunninghake | Zendy

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Adenoviral Infection Decreases Mortality from Lipopolysaccharide-Induced Liver Failure Via Induction of TNF-α Tolerance

Author(s) -

Timur O. Yarovinsky,

Linda S. Powers,

Noah S. Butler,

Mary A. Bradford,

Martha M. Monick,

Gary W. Hunninghake

Publication year - 2003

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.171.5.2453

Subject(s) - tumor necrosis factor alpha , fulminant , in vivo , lipopolysaccharide , adenoviridae , adenovirus infection , immunology , medicine , stimulation , fulminant hepatitis , virology , biology , hepatitis , gene , genetic enhancement , virus , biochemistry , microbiology and biotechnology

Effects of adenoviral infection on in vivo responses to LPS mediated by TNF-alpha were evaluated in a murine model. Adenovirus-infected mice showed decreased mortality from fulminant hepatitis induced by administration of LPS or staphylococcal enterotoxin B in the presence of D-galactosamine. Importantly, TNF-alpha resistance genes within adenoviral E3 region were not required, because E1,E3-deleted vectors showed similar effects. Adenovirus-infected mice exhibited higher TNF-alpha levels after LPS stimulation, no difference in TNFR1 expression, and similar mortality from Fas-induced fulminant hepatitis. Decreased production of IL-6 and KC in response to exogenous TNF-alpha, in addition to protection from TNF-alpha, suggested that adenoviral infection results in TNF-alpha tolerance.

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