Inflammation can be triggered by various insults, such as infection, tissue injury, and cellular stress. This first line defense mechanism rapidly triggers the release of pro-inflammatory substances, including cytokines, free radicals, hormones and other small molecules to combat the stressor by initiating inflammation-resolving processes such as the adaptive immune response1. However, a number of other cells also participate in the concerted effort to limit and repair tissue injury. For example, damage to endothelial cells can result in the activation of the complement system and the release of thrombin, which leads to subsequent initiation of the coagulation factor cascade, platelet aggregation and clot formation thus contributing to injury repair and tissue remodeling1-3.
Various transcription factors including nuclear factor kappa B (NF-KB), activator protein 1 (AP-1) and early growth response 1 (EGR-1) induce the expression of gene products integral to the inflammatory response thus controlling the production of inflammatory mediators, while also indirectly contributing to the activation of the cells involved2.
While this acute inflammatory response can lead to pathological consequences, it is in itself not a disease but a means to maintain homeostasis, and how the response is eventually executed typically depends on the original trigger. However, if resolution of the acute inflammation is not achieved, chronic exposure or ongoing stress leads to chronic inflammation and the development of smoking-related diseases4,5.