| Mechanism of IL-6-mediated cardiac dysfunction following trauma-hemorrhage. | |
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MedLine Citation:
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PMID: 16499925 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cardiac function is depressed and circulating IL-6 levels increase following trauma-hemorrhage (T-H). Although sustained elevated IL-6 after T-H correlate with poor outcome, the mechanism by which IL-6 produces cardiac dysfunction remains unknown. We hypothesized that IL-6-mediated cardiac depression is due to upregulation of NF-small ka, CyrillicB, ICAM, CINC and neutrophil infiltration. Six groups of male adult rats (275-300 g) were used: sham/T-H + vehicle, sham/T-H + IgG, sham/T-H + anti-IL-6mAb. Following midline laparotomy, 60% of the circulating blood was withdrawn and after 90 min, crystalloid fluid resuscitation was provided. Either normal goat IgG or anti-rat IL-6mAb (16.7 microg/kg BW) was administered intraperitoneally at 30 min after the onset of resuscitation. Two hours after resuscitation, cardiac function was measured, blood samples collected, cardiomyocytes isolated and intracellular IL-6 levels measured by flow cytometry. Cardiac IL-6, IL-6R, gp130, NF-small ka, CyrillicB, Ismall ka, CyrillicB-alpha, and ICAM-1 protein levels were measured in freshly isolated hearts by immunoblotting. Moreover, cardiac MPO activity and CINC-1 and -3 were measured. Cardiac function was depressed and cardiac IL-6, NF-small ka, CyrillicB, ICAM-1, MPO activity, and CINC-1 and -3 were markedly increased after T-H. Administration of anti-IL-6mAb following T-H: 1) improved cardiac output (P<0.05); 2) downregulated cardiac IL-6 levels (P<0.05); 3) attenuated cardiac NF-small ka, CyrillicB, ICAM-1, CINC-1, -3, and MPO activity (P<0.05). Administration of IgG, however, did not significantly influence these parameters. Thus, IL-6-mediated upregulation of cardiac NF-small ka, CyrillicB, ICAM-1, CINC-1, -3, and MPO activity likely contributes to altered cardiac function following T-H and neutralization of IL-6 therefore appears to be an effective and novel adjunct for improving organ/cell function under those conditions. |
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Authors:
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Shaolong Yang; Shunhua Hu; Ya-Ching Hsieh; Mashkoor A Choudhry; Loring W Rue; Kirby I Bland; Irshad H Chaudry |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2006-02-24 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 40 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2006 Apr |
Date Detail:
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Created Date: 2006-03-27 Completed Date: 2006-06-13 Revised Date: 2010-04-01 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 570-9 Citation Subset: IM |
Affiliation:
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Center for Surgical Research and Department of Surgery, The University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall, Room G094, Birmingham, AL 35294-0019, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibodies / administration & dosage, immunology Gene Expression Regulation* / drug effects, immunology Interleukin-6 / blood*, immunology Male Myocardium / immunology, metabolism*, pathology Neutrophil Infiltration* / drug effects, immunology Rats Rats, Sprague-Dawley Shock, Hemorrhagic / blood*, immunology, pathology Wounds and Injuries / blood*, immunology, pathology |
| Grant Support | |
ID/Acronym/Agency:
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R37 GM39519/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antibodies; 0/Interleukin-6 |
| Comments/Corrections | |
Erratum In:
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J Mol Cell Cardiol. 2010 Feb;48(2):428 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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