NDLI: Hydrogen sulfide increases survival during sepsis: Protective effect of CHOP inhibition

Content Provider	PubMed Central
Author	Ferlito, Marcella Wang, Qihong Fulton, William B. Colombani, Paul Marchionni, Luigi Karen, Fox-talbot Nazareno, Paolocci Steenbergen, Charles
Abstract	Sepsis is a major cause of mortality, and dysregulation of the immune response plays a central role in this syndrome. Hydrogen sulfide (H2S), a recently discovered gaso-transmitter, is endogenously generated by many cell types, regulating a number of physiologic processes and pathophysiologic conditions. Here we report that H2S increased survival after experimental sepsis induced by cecal ligation and puncture (CLP) in mice. Exogenous H2S decreased the systemic inflammatory response, reduced apoptosis in the spleen, and accelerated bacterial eradication. We found that CHOP, a mediator of the endoplasmic reticulum (ER) stress response, was elevated in several organs after CLP and its expression was inhibited by H2S treatment. Using CHOP knockout (KO) mice, we demonstrated for the first time that genetic deletion of Chop increased survival after lipopolysaccharide (LPS) injection or CLP. CHOP KO mice displayed diminished splenic caspase-3 activation and apoptosis, decreased cytokine production and augmented bacterial clearance. Furthermore, septic CHOP KO mice treated with H2S showed no additive survival benefit compared to septic CHOP KO mice. Finally, we showed that H2S inhibited CHOP expression in macrophages by a mechanism involving Nrf2 activation. In conclusion, our findings show a protective effect of H2S treatment afforded, at least partially, by inhibition of CHOP expression. The data reveal a major negative role for the transcription factor CHOP in overall survival during sepsis and suggest a new target for clinical intervention as well potential strategies for treatment.
Related Links	http://dx.doi.org/10.4049/jimmunol.1300835
Ending Page	1814
Page Count	9
Starting Page	1806
File Format	PDF
ISSN	00221767
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	4
Volume Number	192
Language	English
Publisher Date	2014-02-15
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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