Toll-like receptor-mediated inflammation markers are strongly induced in heart tissue in patients with cardiac disease under both ischemic and non-ischemic conditions
| Autor: | Göran Bergström, Michaela Johansson, Lillemor Mattsson Hultén, Annika Lundqvist, Joakim Sandstedt, Victoria Rotter Sopasakis, Anders Jeppsson |
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| Rok vydání: | 2019 |
| Předmět: |
Male
Heart Diseases Myocardial Ischemia Inflammation Disease 030204 cardiovascular system & hematology 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Humans Medicine 030212 general & internal medicine Coronary Artery Bypass Receptor Toll-like receptor Innate immune system business.industry Gene Expression Profiling Pathogen-associated molecular pattern Toll-Like Receptors Middle Aged Immunity Innate Up-Regulation medicine.anatomical_structure Aortic Valve Immunology Female Inflammation Mediators medicine.symptom Cardiology and Cardiovascular Medicine business Signal Transduction Artery |
| Zdroj: | International Journal of Cardiology. 293:238-247 |
| ISSN: | 0167-5273 |
| Popis: | Background A sustained low grade inflammatory state is a recognized feature of various diseases, including cardiovascular disease. This state of chronic inflammation involves activation of Toll-like receptor (TLR) signaling. However, little is known regarding the genetic profile of TLR components in cardiac tissue from patients with cardiac disease. Methods In this study we investigated the genetic profile of 84 TLR markers in a unique set of cardiac tissue from patients that had undergone either coronary artery bypass grafting (CABG) or aortic valve replacement (AVR). In addition, we compared the gene data from the cardiac tissue with the same gene profile in blood as well as circulating cytokines to elucidate possible targets in blood that could be used to estimate the inflammatory state of the heart in cardiac disease. Results We found a marked upregulation of TLR-induced inflammation in cardiac tissue from both patient groups compared to healthy controls. The inflammation appeared to be primarily mediated through TLR1, 3, 7, 8 and 10, resulting in a marked induction of mediators of the innate immune response. Furthermore, the gene expression data in combination with unbiased multivariate analysis suggested a difference in inflammatory response in ischemic cardiac tissue compared to non-ischemic cardiac tissue. Serum levels of IL-13 were significantly elevated in both CABG and AVR patients compared to controls, whereas other cytokines did not appear to coincide with cardiac TLR-induced inflammation. Conclusions We propose that cardiac disease in humans may be mediated by local cardiac TLR signaling under both ischemic and non-ischemic conditions. |
| Databáze: | OpenAIRE |
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