Atherosclerosis and Interleukin-1 Beta: Is the Link?
Andrejus Coj, Eglė Totmianinienė
Summary
During the past decade, several novel risk factors for atherosclerosis (including inflammation, infections, response to violation and trauma theory) have been reported. Cells involved in the atherosclerotic process secrete and are activated by soluble factors, known as cytokines and interleukin-1 (IL-1) one of the main pro- atherogenic cytokines. IL-1p primary product, 30.7 kDa amino acids protein is not active and only after proteolytic enzyme caspase cleavage becomes active 17kDa protein. IL-ip is secretory form of IL-1. Generally physiological conditions affect cleavage of IL-1p N-terminal protein. In case of cell apoptosis or injury, enzymes known as trypsin, elastase, chymotrypsin, mast cells chimase, and other proteases can cleave N-terminal protein and activate IL-ip. IL-ip binding IL-1RI receptor and form complex which associate with IL-1 receptor accessory protein. Only IL-ip:IL-1RI:IL-1R-AcP complex can initiate cell signaling paths. Inflammation and inj ury are crucial components for athero- genesis. In this article reviewed newest available data about IL-1, correspondence and differences of different IL-1 types, overviewed IL-1p, and looked for relation between IL-1p and atherosclerosis. Presented data about IL-1p and inflammation processes which affects complex pathways associated with inflamma- some formation, cholesterol crystal role to activate inflammation processes. Some newest experimental data about genetic polymorphisms of IL-1p and relation with atherosclerosis, IL-1p correlation with M-CSF, IL-8, IL-6, IL-1Ra and other markers also presented. Information about the LITGEN project, its main aims, tasks and plans is presented.
Keywords: IL-1p, inflammation, atherosclerosis.