[논문]A Role for IFN-αβ in Virus Infection-Induced Sensitization to Endotoxin

Doughty, Lesley A.; Nguyen, Khuong B.; Durbin, Joan E.; Biron, Christine A.

doi:10.4049/jimmunol.166.4.2658

[해외논문] A Role for IFN-αβ in Virus Infection-Induced Sensitization to Endotoxin 원문보기

The journal of immunology : official journal of the American Association of Immunologists, v.166 no.4, 2001년, pp.2658 - 2664

Doughty, Lesley A. (*Pediatrics and) , Nguyen, Khuong B. (†Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912) , Durbin, Joan E. (and) , Biron, Christine A. (‡Division of Pediatric Pathology, Department of Pediatrics, College of Medicine and Public Health, Ohio State University, Columbus, OH 43210)

Abstract ▼ AI-Helper

AbstractUnderlying viral infections can heighten sensitivity and worsen cytokine-mediated disease following secondary inflammatory challenges. Mechanisms for this are poorly understood. The impact of the innate response to lymphocytic choriomeningitis virus (LCMV) infection on sensitivity to endotoxin (LPS) was investigated. Compared with uninfected mice, infection with LCMV for 2-days-sensitized mice to LPS by ∼2-fold for lethality and by 2- to 6-fold for serum TNF-α levels. Priming for LPS-induced TNF-α was also seen with splenic and peritoneal leukocytes isolated from infected mice and challenged with LPS ex vivo. The effect on TNF-α production was present in the absence of IFN-γ, its major producers NK and T cells, and the major pathways for its induction through IL-12 and the signal transducer and activator of transcription 4 (STAT4), and therefore was IFN-γ independent. Early LCMV infection induces high concentrations of the type 1 IFNs, IFN-αβ. Administration of recombinant IFN-α alone heightened the TNF-α response to LPS. Innate IFN-αβ and IFN-γ responses to LCMV exist in a delicate balance. To reduce priming for LPS-induced TNF-α during LCMV, deficiencies in both the IFN-αβ and IFN-γ receptors or STAT1, a transcription factor downstream to both IFNs, were required. These data demonstrate that early viral infection can enhance sensitivity to bacterial products, and that this sensitization can occur in part as a result of endogenously expressed IFN-αβ. This work also raises issues about potential complications associated with IFN-αβ therapies.

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