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Toll-like receptor-mediated inflammation markers are strongly induced in heart tissue in patients with cardiac disease under both ischemic and non-ischemic conditions.

Int J Cardiol. 2019 Jun 14;:

Authors: Rotter Sopasakis V, Sandstedt J, Johansson M, Lundqvist A, Bergström G, Jeppsson A, Mattsson Hultén L

Abstract
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.

PMID: 31230935 [PubMed – as supplied by publisher]

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