Elevated plasma levels of interleukin-16 in patients with acute myocardial infarction.
Medicine (Baltimore)
; 96(44): e8396, 2017 Nov.
Article
em En
| MEDLINE
| ID: mdl-29095267
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, nâ=â45) and without ST-segment elevation myocardial infarction (NSTEMI, nâ=â42) compared with controls with excluded coronary artery disease (nâ=â55). 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 759.38â±â471.54, NSTEMI 677.77â±â438.8, control 500.45â±â432.21; Pâ=â.002). IL-16 correlated with CRP (râ=â0.26, Pâ=â.001), leucocytes (râ=â0.38, Pâ<â.001), NT-proBNP (râ=â0.20, Pâ=â.02) and hsTnT (râ=â0.25, Pâ=â.004). Circulating myeloid DCPs, plasmacytoid DCPs, and total DCPs showed a significant inverse correlation to IL-16 levels (râ=â-0.21, Pâ=â.01; râ=â-0.23, Pâ=â.005; râ=â-0.26, Pâ=â.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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Interleucina-16
/
Infarto do Miocárdio sem Supradesnível do Segmento ST
/
Infarto do Miocárdio com Supradesnível do Segmento ST
Tipo de estudo:
Diagnostic_studies
/
Observational_studies
Limite:
Female
/
Humans
/
Male
/
Middle aged
Idioma:
En
Revista:
Medicine (Baltimore)
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
Áustria