title: Chronic inflammation in asthma: a contest of persistence vs resolution.
abstract: Recent investigations have highlighted that endogenous anti-inflammatory mediators and immune regulating mechanisms are important for the resolution of inflammatory processes. A disruption of these mechanisms can be causally related not only to the initiation of unnecessary inflammation, but also to the persistence of several chronic inflammatory diseases. In asthma, chronic Th-2 driven eosinophilic inflammation of the airways is one of the central abnormalities. To date, elucidating the role of the different pro-inflammatory mediators involved in orchestrating the inflammatory processes in asthma has been the subject of intense research in both humans and animal models. However, the counter-regulatory mechanisms that co-determine the outcome in the contest of resolution vs persistence of the eosinophilic airway inflammation remain poorly understood. These are currently being investigated in animal models of chronic asthma. Elucidating these mechanisms is of relevance, since it can give rise to a new therapeutic approach in the treatment of chronic airway inflammation in asthmatics. This novel concept of treatment involves the stimulation of endogenous anti-inflammatory pathways, rather than solely antagonising the various pro-inflammatory mediators. Here, we review and discuss the current knowledge about these endogenous anti-inflammatory mediators in clinical and experimental asthma.
authors.affiliation: Department of Respiratory Medicine, Laboratory of Translational Research in Obstructive Pulmonary Diseases, Ghent University, Ghent, Belgium.
authors.forename: C L
authors.initials: CL
authors.lastname: Van Hove
authors.forename: T
authors.initials: T
authors.lastname: Maes
authors.forename: G F
authors.initials: GF
authors.lastname: Joos
authors.forename: K G
authors.initials: KG
authors.lastname: Tournoy
mesh_terms: D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D002908:Chronic Disease; D004802:Eosinophilia; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*