Thermal hyperalgesia: animals were held in Perspex enclosures with a glass floor

the same therapeutic measures. This type of varied presentation and differential response to the same treatment is at times baffling and suggests that the involvement of various organs and tissues due to the underlying inflammatory process is varied, and the degree of involvement may differ in both time and extent and, more importantly, is unpredictable. It is also possible that continued inflammatory events seen in lupus, rheumatoid arthritis, and other rheumatological conditions could be due to failure of the resolution of inflammation. Thus, the balance between inflammation and resolution is disturbed more in favor of proinflammatory events and/or failure of resolution-inducing molecules to be produced at the most appropriate time, leading to nonresolution of inflammation. In other words, even after the inciting agent responsible for the initiation of inflammation is removed, inappropriate inflammation continues simply because resolution failed to occur. This leads to delay in the healing/repair process and so tissue/organ damage continues. This may explain why target organ damage continues even when these patients are continuing to take anti-inflammatory and immunosuppressive medicines. In view of this, it is imperative that administration of proresolution-inducing agents is needed to obtain full remission and restore normal A-83-01 supplier physiological function of the target tissues/organs in these diseases. Such endogenous proresolution-inducing molecules include lipoxins, resolvins, protectins, maresins, NO, nitrolipids, 15 deoxy1214 PGJ2, PGD2, anti-inflammatory cytokines such as IL-4, IL-10, and some polyunsaturated fatty acids. Hence, understanding the interaction between proinflammatory and anti-inflammatory and proresolution molecules is important to devise newer therapeutic strategies in several inflammatory conditions. O2- H2O2 Fe++ RNI OH Pathobiology of inflammation with specific reference to chronic inflammation Inflammation is a reaction to injurious agents, either external or internal, that consists of both vascular and cellular responses. Inflammation may be local or systemic, and it can be acute or chronic. During inflammation, the reaction of blood vessels is unique and leads to the accumulation of fluid and leukocytes in extravascular tissues. This reaction can be in the form of vasodilatation, which is seen as hyperemia at the site of injury and which serves the essential function of increasing the blood supply to the injured tissue/organ so that Journal of Inflammation Research 2010:3 Inflammation 144 Dovepress Dovepress Current and emerging strategies for the treatment and management of SLe Diet adequate elimination of the inflammation-inducing agent is achieved and/or the repair process can occur after the inflammation subsides. Thus, injury and repair are two faces of the inflammatory process, and it is difficult to separate these two processes. In fact, in the majority of instances, inflammation to injury and repair occur almost simultaneously.1 -6 Series Cis-linoleic acid Desaturase 6 -3 Series -Linolenic acid Mediators of inflammation Some of the important mediators of inflammation include histamine, serotonin, lysosomal enzymes, PGs, LTs, PAFs, ROS, NO, HOCL, various cytokines, kinin system, coagulation/ fibrinolysis system, and complement system.1 The role of arachidonic acid and other PUFAs and their products in inflammation deserves special mention in view of their role in inflammation, resolution PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19836835 of inflammation, an