NDLI: Protective role of reactive oxygen species in endotoxin-induced lung inflammation through modulation of IL-10 expression.

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Protective role of reactive oxygen species in endotoxin-induced lung inflammation through modulation of IL-10 expression.

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Comment on 'Cutting edge: regulatory T cells do not mediate suppression via programmed cell death pathways'.

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Protective role of reactive oxygen species in endotoxin-induced lung inflammation through modulation of IL-10 expression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Karpurapu, Manjula Christman, John W. Deng, Jing Wang, Xuerong Qian, Feng Vogel, Stephen Park, Hyesuk Ye, Richard D. Park, Gye Young Xiao, Lei Ranjan, Ravi
Description	Country affiliation: United States Author Affiliation: Deng J ( Section of Pulmonary, Critical Care, Sleep, and Allergy, Department of Medicine, University of Illinois, Chicago, IL 60612, USA.)
Abstract	Reactive oxygen species (ROS) generated by NADPH oxidase are generally known to be proinflammatory, and it seems to be counterintuitive that ROS play a critical role in regulating the resolution of the inflammatory response. However, we observed that deficiency of the p47(phox) component of NADPH oxidase in macrophages was associated with a paradoxical accentuation of inflammation in a whole animal model of noninfectious sepsis induced by endotoxin. We have confirmed this observation by interrogating four separate in vivo models that use complementary methodology including the use of p47(phox-/-) mice, p47(phox-/-) bone marrow chimera mice, adoptive transfer of macrophages from p47(phox-/-) mice, and an isolated perfused lung edema model that all point to a relationship between excessive acute inflammation and p47(phox) deficiency in macrophages. Mechanistic data indicate that ROS deficiency in both cells and mice results in decreased production of IL-10 in response to treatment with LPS, at least in part, through attenuation of the Akt-GSK3-ß signal pathway and that it can be reversed by the administration of rIL-10. Our data support the innovative concept that generation of ROS is essential for counterregulation of acute lung inflammation.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1101323
Journal	The Journal of Immunology
Issue Number	11
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Endotoxins Toxicity Gene Expression Regulation Immunology Interleukin-10 Biosynthesis Lung Pathology Pneumonia Reactive Oxygen Species Therapeutic Use Adoptive Transfer Animals Disease Models, Animal Antagonists & Inhibitors Luciferases Genetics Metabolism Macrophages, Peritoneal Transplantation Mice Mice, Knockout Mice, Transgenic Nadph Oxidase Deficiency Therapy Recombinant Proteins Administration & Dosage Research Support, N.i.h., Extramural Research Support, U.s. Gov't, Non-p.h.s. Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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