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Elevated plasma levels of interleukin-16 in patients with acute myocardial infarction
Christiana Schernthaner1, Vera Paar, Bernhard Wernly
1Department of Cardiology, Paracelsus Medical University, Salzburg, Austria Department of Internal Medicine I, Division of Cardiology, Angiology, Pneumology and Intensive MedicalCare, Friedrich-Schiller-University Jena, Jena, Germany Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf, Germany Department of Laboratory Medicine, Paracelsus Medical University, Salzburg, Austria.
Abstract:
Interleukin (IL)-16, a polypeptide cytokine, plays a crucial role in the inflammatory process, acting as a chemoattractant for peripheral immune cells and has been linked to various inflammatory diseases. However, its role in patients with acute myocardial infarction (AMI) is unclear.We retrospectively analyzed serum levels of IL-16 in blood of patients with (STEMI, n = 45) and without ST-segment elevation myocardial infarction (NSTEMI, n = 42) compared with controls with excluded coronary artery disease (n = 55). Furthermore, correlation analysis with inflammatory cells, C-reactive protein (CRP) levels, dendritic cell precursors (DCPs), and other clinical and biochemical markers was performed.Compared with controls, patients with STEMI and NSTEMI evidenced higher levels of IL-16 in pg/mL (STEMI: 759.38 ± 471.54, NSTEMI: 677.77 ± 438.8, control: 500.45 ± 432.21; P = .002). IL-16 correlated with CRP (r = 0.26, P = .001), leucocytes (r = 0.38, P < .001), NT-proBNP (r = 0.20, P = .02) and hsTnT (r = 0.25, P = .004). Circulating myeloid DCPs, plasmacytoid DCPs, and total DCPs showed a significant inverse correlation to IL-16 levels (r = -0.21, P = .01; r = -0.23, P = .005; r = -0.26, P = .002, respectively).Interleukin-16 might play an important role in the inflammatory process of patients suffering from AMI and correlates with inflammatory cell activation and clinical and biochemical markers. The cytokine IL-16 might upregulate the proinflammatory response and recruitment of inflammatory cells into infarcted myocardium.
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