Derangement in Homeostasis of Neutrophil Elastase and its Inhibitory Systems in Ischemic Stroke Patients
Mamatha Kunder1*
, A.V. Moideen Kutty2 and V. Lakshmaiah3 1Department of Biochemistry, Yenepoya School of Allied Health Sciences, Yenepoya (Deemed to be) University, Mangalore, Karnataka, India.
2Yenepoya (Deemed to be) University, Mangalore, Karnataka, India.
3Department of Medicine, Sri Devaraj Urs Medical College, Sri Devaraj Urs Academy of Higher Education and Research, Kolar, Karnataka, India.
Corresponding Author E-mail: mamathayogesh79@gmail.com
Abstract: Neutrophils are the first to infiltrate ischemic brain regions causing the release of Neutrophil Elastase (NE), a pro-inflammatory proteinase. The activity of NE is well regulated by endogenous inhibitors alpha1-antitrypsin (α1-AT) and alpha2-macroglobulin (α2-MG). The physiological balance of elastase and anti-elastase factors is essential to maintain the normal integrity of tissues and an imbalance has been implicated in the pathogenesis of several acute and chronic inflammatory diseases. The present study was designed to determine the plasma levels of NE, α1-AT, α2-MG, and NE–α1-AT complex to evaluate their role in inflammatory processes of ischemic stroke. The effect of homocysteine on the release of elastase from neutrophils was also studied. The study involved a total of 100 subjects (controls =60 and patients=40). Significantly higher mean elastase activity and lower α1-AT levels were observed in ischemic stroke patients than in controls. NE- α1-AT complex and α2-MG levels were significantly increased in the patient group. The in vitro study indicated homocysteine induced release of elastase from neutrophils. In conclusion, homeostasis of NE and its endogenous inhibitors is deranged in patients suggestive of their role in the pathogenesis of ischemic stroke through exacerbating inflammatory and coagulation processes.
Keywords: α1-Antitrypsin; α2-Macroglobulin; Acute Ischemic Stroke; Homocysteine; Neutrophil Elastase Back to TOC