Role of interleukin-6 in regulation of immune responses to remodeling after myocardial infarction

Abstract

Myocardial remodeling following myocardial infarction (MI) is emerging as key causes of chronic infarct mortality. Interleukin-6 is a classic pro-inflammatory cytokine needed to mount an effective immune response. It seems that interleukin-6 acts as an important role in the dynamic and superbly orchestrated process of innate immunity after MI. Interleukin-6 timely suppresses of innate immune signals to prevent the catastrophic consequences of uncontrolled inflammation on cardiac geometry and function, and thus tunes myocardial remodeling. A comprehensive understanding of biological processes of interleukin-6 in innate immunity leading to inflammatory response and disease-related ventricular remodeling is helpful to find the solution of chronic heart failure. To accomplish this, we reviewed the articles of interleukin-6 regard to inflammation, innate immunity, and cardiac remodeling. This review focuses on the role of interleukin-6 that dominates cell-mediated immunity, especially on neutrophils, monocytes, macrophages, and fibroblasts. In addition, we will also briefly discuss other inflammatory cytokines involved in this process within the paper.

Titin-Based Cardiac Myocyte Stiffening Contributes to Early Adaptive Ventricular Remodeling After Myocardial Infarction

“…IL-6 is a multifunctional cytokine involved in the regulation of immune responses 1 and has been implicated in cardiac remodeling. 30 IL-6 is highly expressed in the LV within the first 24 hours after MI, and its plasma and LV tissue levels remain elevated for the first 3 days post MI.…”

“…Permanent Myocardial ischemia C57/BL6J mice were anesthetized by intra-peritoneal injection of ketamine (60 mg/kg BW) and xylazine (10 mg/kg BW), as previously described 1 . After anesthesia was sufficient (confirmed by squeezing the paws) animals were intubated and connected to a rodent ventilator (Minivent Microventilator, Hugo Sachs, Germany).…”

“…After mice regained spontaneous breathing they were extubated. Echocardiography Cardiac images were acquired using a Vevo 2100 high-resolution ultrasound scanner with 18-38 MHz linear transducer (VisualSonics Inc.) pre MI and 3 days post MI respectively 10 days post MI as previously described 1,2 . Echocardiography was performed under slight mask anesthesia by an inhaled mixture of 1.5% (v/v) isoflurane and 100% oxygen.…”

The Role of Inflammation in Myocardial Infarction

“…IL-6 is also an important proinflammatory cytokine that is closely associated with CRP levels. Following MI, its levels are increased within 1-2 days and it can remain elevated even 3 months afterward [85], stimulating various effects on a wide range of cell types [86]. In addition, IL-10 is an anti-inflammatory cytokine, which along with TGF-β plays an important role in the inhibition of the inflammatory phase and in the initiation of the granulation phase.…”

Hesperetin protects against inflammatory response and cardiac fibrosis in postmyocardial infarction mice by inhibiting nuclear factor κB signaling pathway

“…An early study has found that application of reduced the degree of MI glucocorticoids in dogs due to their anti-inflammatory action, which proves that inflammation has a critical role in MI (3). Subsequent studies have found that macrophages, T lymphocytes, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 all have important roles in the area of MI and the deterioration of cardiac function after MI (4)(5)(6). Proinflammatory factors, including TNF-α, IL-1β and IL-6, are not continuously expressed in normal myocardial tissue, and the production or up-regulated expression of these factors represents an internal resistance to myocardial injury (1).…”