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Cardiopulmonary alterations in mRNA expression for interleukin‐1β, the interleukin‐6 superfamily and CXC‐chemokines during development of postischaemic heart failure in the rat
Author(s) -
Tønnessen Theis,
Florholmen Geir,
Henriksen Unni Lie,
Christensen Geir
Publication year - 2003
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1046/j.1475-097x.2003.00503.x
Subject(s) - medicine , downregulation and upregulation , chemokine , ciliary neurotrophic factor , proinflammatory cytokine , interleukin , endocrinology , ventricle , heart failure , cytokine , immunology , cardiology , inflammation , receptor , biology , neurotrophic factors , biochemistry , gene
Summary Cytokines and chemokines are believed to play a pathogenic role in heart failure (HF). Although some cytokines and chemokines have been examined in HF, information about others is still lacking. We aimed to examine the expression of cytokines belonging to the interleukin (IL)‐6 superfamily [IL‐6 and ciliary neurotrophic factor (CNTF)], as well as IL‐1 β and the CXC‐chemokines monocyte chemoattractant protein‐1 (MCP‐1) and IL‐8. We examined their expression in the heart, lung and spleen during development of postischaemic HF 1 and 6 weeks following left coronary artery ligation. Rats, which after myocardial infarction had a left ventricular end‐diastolic pressure above 15 mmHg, were considered to be in HF. Sham‐operated rats served as controls. A substantial upregulation of cardiac IL‐1 β was measured in HF at 1 week, whereas a downregulation was measured in the lungs. At 6 weeks no altered regulation was seen. CNTF was only upregulated in the viable left ventricle at 6 weeks and IL‐6 was upregulated in the infarcted region at 1 week. Cardiac MCP‐1 was upregulated in the viable and the infarcted region of the failing left ventricle at 1 week, with the highest expression in the latter. In the lung, another pattern of regulation was seen with a significant increase in pulmonary MCP‐1 at 6 weeks. IL‐8 was only detected in the infarcted region at 1 week. In the spleen, no regulation of cytokines was found. In conclusion, we report an organ‐specific regulation of cytokines and chemokines in postischaemic HF. Our novel findings of increased cardiac CNTF and cardiopulmonary MCP‐1 mRNA indicate a role for these factors in the pathogenesis of HF.