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Journal of Endotoxin Research
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The role of STAT1 in viral sensitization to LPS

Joan Durbin

Department of Pediatrics, Columbus Children's Research Institute, The Ohio State University Columbus, Ohio, USA, durbinj{at}pediatrics.ohio-state.edu

Leslie Doughty

Department of Pediatrics, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island, USA

Ken Nguyen

Department of Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, Rhode Island, USA

Michael Caligiuri

Department of Internal Medicine, Division of Hematology Oncology, The Ohio State University, Columbus, Ohio, USA

Jeff Van Deusen

Department of Internal Medicine, Division of Hematology Oncology, The Ohio State University, Columbus, Ohio, USA

Christine Biron

Department of Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, Rhode Island, USA

The phenomenon of endotoxin sensitization by virus infection is well documented but not yet well understood. Infection by virtually any viral agent will quickly induce expression of type I interferons (IFN-{alpha}/ß), and type II IFN-{gamma} production will follow as NK cells and T cells are activated. It has been well established that type II IFN pretreatment can intensify the effects of endotoxin. We have recently demonstrated that type I IFN induction by lymphocytic choriomeningitis virus (LCMV) infection dramatically increases TNF-{alpha} production following LPS treatment, and that this sensitization by type I IFN is STAT1 dependent. Taken together these data suggest that the STAT1-mediated, MyD88-independent, arm of the LPS signaling pathway plays an important role in endotoxin toxicity, and that this pathway mediates a major component of virus-enhanced LPS sensitization.

Journal of Endotoxin Research, Vol. 9, No. 5, 313-316 (2003)
DOI: 10.1177/09680519030090050701
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