NDLI: A critical role for human caspase-4 in endotoxin sensitivity.

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A critical role for human caspase-4 in endotoxin sensitivity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Schiff, Tamar Voloudakis, Georgios Gama Sosa, Miguel A. Elder, Gregory Buxbaum, Joseph D. Bozdagi, Ozlem Kajiwara, Yuji
Description	Author Affiliation: Kajiwara Y ( Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029); Schiff T ( Baylor College of Medicine, Houston, TX 77030); Voloudakis G ( Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029); Gama Sosa MA ( Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029); Elder G ( Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029); Bozdagi O ( Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029); Buxbaum JD ( Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029)
Abstract	Response to endotoxins is an important part of the organismal reaction to Gram-negative bacteria and plays a critical role in sepsis and septic shock, as well as other conditions such as metabolic endotoxemia. Humans are generally more sensitive to endotoxins when compared with experimental animals such as mice. Inflammatory caspases mediate endotoxin-induced IL-1ß secretion and lethality in mice, and caspase-4 is an inflammatory caspase that is found in the human, and not mouse, genome. To test whether caspase-4 is involved in endotoxin sensitivity, we developed a transgenic mouse expressing human caspase-4 in its genomic context. Caspase-4 transgenic mice exhibited significantly higher endotoxin sensitivity, as measured by enhanced cytokine secretion and lethality following LPS challenge. Using bone marrow-derived macrophages, we then observed that caspase-4 can support activation of caspase-1 and secretion of IL-1ß and IL-18 in response to priming signals (LPS or Pam3CSK4) alone, without the need for second signals to stimulate the assembly of the inflammasome. These findings indicate that the regulation of caspase-1 activity by human caspase-4 could represent a unique mechanism in humans, as compared with laboratory rodents, and may partially explain the higher sensitivity to endotoxins observed in humans. Regulation of the expression, activation, or activity of caspase-4 therefore represents targets for systemic inflammatory response syndrome, sepsis, septic shock, and related disorders.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1303424
Journal	The Journal of Immunology
Issue Number	1
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Caspases, Initiator Immunology Caspases Lipopeptides Toxicity Lipopolysaccharides Macrophages Animals Genetics Cell Line Enzyme Induction Drug Effects Inflammasomes Interleukin-18 Interleukin-1beta Mice Mice, Knockout Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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A critical role for human caspase-4 in endotoxin sensitivity.

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