Resolution of inflammation: from basic concepts to clinical application

Excerpt

Acute inflammation may protect the body from invading bacteria or viruses and can help to overcome injuries. While such acute inflammatory processes are usually self-limiting and are followed by tissue repair and healing responses, there are some circumstances in which acute inflammation fails to resolve and is subsequently followed by development of chronic inflammation [1, 2]. Chronic inflammatory disorders place a major burden [3, 4] on affected patients and the responsible health care systems. Key inflammatory disorders in this context comprise various diseases such as psoriasis [5], pemphigus vulgaris [6], graft versus host disease [7], allergic asthma [8], rheumatoid arthritis [9], lupus erythematosus [10], neuroinflammatory disorders [11] and multiple sclerosis [12], uveitis [13], Crohn’s disease [14], and ulcerative colitis [15]. In addition, atherosclerosis has been identified as a lipid-driven inflammatory disease [16]. Collectively, the above chronic disorders are frequently detected in Western societies [17‐27]. They are quite problematic for affected patients, as they may induce tissue alterations and progressive tissue destruction (e.g., bone and cartilage destruction in rheumatoid arthritis) or can induce organ failure (e.g., kidney failure in lupus erythematosus) [19, 28]. Furthermore, chronic inflammation may predispose to cancer. In fact, about 20% of cancer cases in humans are caused by chronic inflammation (e.g., colon cancer in inflammatory bowel diseases) [29, 30]. Moreover, cancer is frequently associated with a chronic inflammatory response in the local microenvironment and such inflammation may profoundly control tumor growth and prognosis [31‐33]. These observations underline the unmet clinical need to gain further detailed insights into the pathomechanisms of chronic inflammation and into the signalling pathways that impair resolution of inflammation. …