The Role of IL-6 in Ischemic Stroke

Abstract

The pathophysiology of a stroke is a complex process involving oxidative stress and inflammation. As a result of the actions of reactive oxygen species (ROS), not only does vascular damage occur, but the brain tissue is also damaged. It is a dynamic process, induced by a cellular-molecular immune response, focused on the development of an immediate reaction. During ischemia, inflammatory mediators are released, among which IL-6 plays a particularly important role in the acute phase of a stroke. Recently, a lot of attention has been devoted to this pleiotropic pro-inflammatory cytokine, which enhances the migration of leukocytes and is controlled by chemokines and the expression of adhesion handlers. The impact of IL-6 on the severity of neurological treatment and on patient prognosis in AIS is of interest to many researchers. More and more data indicate that it may be a reliable prognostic factor in strokes.

Keywords: biomarker; interleukin 6; ischemic stroke.

Figure 1

IL-6 trans signaling. The IL-6/sIL-6R/gp130 complex can activate intracellular tyrosine kinases that activate STAT transcription factors or the RAS-RAF-MAPK or PI3K pathway. Trans signaling can lead to the expression of a pro-inflammatory state via increased JAK/STAT signaling due to SOCS inhibition. STAT3 phosphorylation can enhance the transcription of genes related to angiogenesis and intense cerebral blood flow. AKT—protein kinase B; IL-4—interleukin 4; IL-6—interleukin 6; JAK—Janus kinase; pg130—signal transducing receptor; PI3K—phosphatidylinositol 3-kinase; RAS—RAF—MAPK—small guanosine triphosphatases—serine/threonine-specific protein—mitogen-activated protein kinases; sIL-6R—soluble isoform of IL-6 receptor; SOCS—proteins called suppressors of cytokine signaling; STAT3—signal transducer and activator of transcription 3; TH1, TH2—lymphocytes; TYK—tyrosine kinase. This figure was created using Servier Medical Art (available at https://smart.servier.com/) (accessed on 12 September 2024).