Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis.

Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Abstract Text:

X Han,N Benight,B Osuntokun,K Loesch,S J Frank,L A Denson,

BACKGROUND: Neutralisation of tumour necrosis factor alpha (TNFalpha) restores systemic growth hormone function in patients with Crohn's disease, and induces mucosal healing. Anabolic effects of growth hormone depend on activation of the STAT5 transcription factor. Although it has recently been reported that both administration of growth hormone and neutralisation of TNFalpha reduce mucosal inflammation in experimental colitis, whether this involved activation of STAT5 in the gut is not known. AIM: To determine whether TNFalpha blockade in colitis up regulates a growth hormone:STAT5 signalling pathway in the colon. METHODS: Interleukin 10-deficient mice and wild-type controls received growth hormone or anti-TNFalpha antibody, and T84 human colon carcinoma cells were treated with TNFalpha or growth hormone. Activation and expression of STAT5b, peroxisome proliferator-activated receptor gamma (PPARgamma), NFkappaB/IkappaB and growth hormone receptor were determined. RESULTS: Growth hormone activated STAT5b and up regulated expression of PPARgamma in normal mouse colon; inflamed colon was partially resistant to this. Chronic administration of growth hormone, nevertheless, significantly reduced activation of colonic NFkappaB (p = 0.028). Neutralisation of TNFalpha rapidly increased abundance of growth hormone receptor, activation of STAT5 and abundance of PPARgamma in the colon, but reduced activation of NFkappaB in colitis. Growth hormone activated STAT5, and directly reduced TNFalpha activation of NFkappaB, in T84 cells. CONCLUSIONS: Reduced activation of colonic STAT5 and expression of PPARgamma may contribute to persistent mucosal inflammation in colitis. Up regulation of STAT5 and PPARgamma, either through neutralisation of TNFalpha or chronic administration of growth hormone, may exert an anti-inflammatory effect in inflammatory bowel disease.

Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Publishing Authors By Initials

X Han,N Benight,B Osuntokun,K Loesch,SJ Frank,LA Denson,

For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

PUBMED ID PMID:

MEDLINE DATE:

Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Gut

VOLUME: 56

Page Numbers: 73-81

Journal Abbreviation: Gut

ISSN: 0017-5749

DAY: 15

MONTH: 06

YEAR: 2006

Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985108

Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Keywords Mesh Terms:

KEYWORDS: Up-Regulation

MESH TERMS: physiology

Chemical & Substance for Abstract: Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis. Information

Substance Name: Interleukin-10

Registry Number: 130068-27-8

Grant and Affiliation Information for Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis.

AFFILIATION: Department of Pediatrics, Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.

Country: England

AGENCY: United States NIDDK

GRANT: R24 DK64403

ACRONYM: DK

MEDLINETA: Gut

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis Related Publications

• Activation of an IL-6:STAT3-dependent transcriptome in pediatric-onset inflammatory bowel disease.
• CYCLOPROPANE.
• Cigarette smoking: a child's guide to addiction.
• Criteria for a standard thromboplastin preparation.
• Fourth report on the standardization of the one-stage prothrombin time for the control of anticoagulant therapy.
• Glittering with gold therapy.
• Proposed specification for a reference thromboplastin preparation for the control of anticoagulant therapy using coumarin type drugs.
• Reaction to gold therapy.
• Second report on the standardisation of the one-stage prothrombin time for the control of anticoagulant therapy.
• Signal transducer and activator of transcription 5b promotes mucosal tolerance in pediatric Crohn's disease and murine colitis.
• Standardization of the one-stage prothrombin time for the control of anticoagulant therapy.
• The establishment and operation of a Nerve Block Clinic; one year's experience at the Los Angeles County Hospital.
• The simplified two-stage assay for Factor 8 using a combined reagent.
• Third report on the standardization of the one-stage prothrombin time for the control of anticoagulant therapy.
• Thromboplastin reference preparations.
• Tumour necrosis factor alpha blockade induces an anti-inflammatory growth hormone signalling pathway in experimental colitis.