Document Detail


COX-2 inhibition attenuates anorexia during systemic inflammation without impairing cytokine production.
MedLine Citation:
PMID:  11832369     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Anorexia and weight loss are frequent complications of acute and chronic infections and result from induction of cytokines, prostaglandins, and other inflammatory mediators that are critical for pathogen elimination. Selective attenuation of the hypophagic response to infection and maintenance of the production of factors essential for infection control would be a useful addition to antimicrobial therapy in the treatment of human disease. Here, we evaluate the relative contribution of cyclooxygenase (COX)-1- and COX-2-derived prostaglandins to anorexia and weight loss precipitated by systemic immune activation by lipopolysaccharide (LPS). Using COX isoform-selective pharmacological inhibitors and gene knockout mice, we found that COX-2 inhibition during LPS-induced inflammation results in preserved food intake and maintenance of body weight, whereas COX-1 inhibition results in augmented and prolonged weight loss. Regulation of neuropeptide Y, corticotropin-releasing hormone, leptin, and interleukin-6 does not change as a function of COX-2 inhibition after LPS administration. Our data implicate COX-2 inhibition as a therapeutic target to maintain nutritional status while still allowing a normal cytokine response during infection.
Authors:
Paulette M Johnson; Sherri K Vogt; Mary W Burney; Louis J Muglia
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  282     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-02-08     Completed Date:  2002-03-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E650-6     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Washington University School of Medicine and St. Louis Children's Hospital, St. Louis, Missouri 63110, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anorexia / etiology,  immunology,  prevention & control*
Corticotropin-Releasing Hormone / genetics
Cyclooxygenase 1
Cyclooxygenase 2
Cyclooxygenase 2 Inhibitors
Cyclooxygenase Inhibitors / pharmacology*
Cytokines / biosynthesis*
Energy Intake
Energy Metabolism
Hypothalamus / chemistry
Immunity
Inflammation / chemically induced,  complications,  immunology*
Isoenzymes / deficiency*,  genetics,  metabolism
Lipopolysaccharides
Male
Membrane Proteins
Mice
Mice, Inbred C3H
Mice, Knockout
Neuropeptide Y / genetics
Prostaglandin-Endoperoxide Synthases / deficiency*,  genetics,  metabolism
Prostaglandins / physiology
Pyrazoles / pharmacology
RNA, Messenger / analysis
Sulfonamides / pharmacology
Weight Loss
Grant Support
ID/Acronym/Agency:
5 T32 HD-07507/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; 0/Cyclooxygenase 2 Inhibitors; 0/Cyclooxygenase Inhibitors; 0/Cytokines; 0/Isoenzymes; 0/Lipopolysaccharides; 0/Membrane Proteins; 0/Neuropeptide Y; 0/Prostaglandins; 0/Pyrazoles; 0/RNA, Messenger; 0/SC 560; 0/Sulfonamides; 9015-71-8/Corticotropin-Releasing Hormone; EC 1.14.99.1/Cyclooxygenase 1; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1/Ptgs1 protein, mouse

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