ABSTRACT
Inammation involving a wide variety of physiological and pathological processes is a kind of body’s immune response against pathogens, toxic chemicals, or physical injury. Symptoms such as redness, heat, swelling, and pain are expressed in the inammatory area that can arise when an injurious agent persists or when the immune system attacks its own tissue. It is largely divided into acute and chronic inammation. Acute inammation is a short-term normal response that usually leads to tissue repair by leukocytes such as macrophages, neutrophils, and eosinophils recruited into the damaged region, removing the cause of inammation by the production of a number of inammatory mediators. In contrast, chronic inammation may progress from acute inammation if the stimuli persist, causing own tissue damage (Drayton et al. 2006). Therefore, chronic inammation is a long-term pathological response that involves tissue destruction due to the incompletion of tissue repair recovered by matrix metalloproteinases (MMPs) inhibitors (Hu et al. 2007). It is well known that the dysregulation of immune response can lead to chronic inammatory diseases, and pharmacological intervention is necessary to attenuate cellular inammatory pathways. Such prolonged inammation ultimately results in several chronic diseases, such as periodontal disease, hepatitis, arthritis, gastritis, colitis, and atherosclerosis. The most important factor in chronic inammation has been known to be the nuclear factor-kappa B (NF-κB) transcription factor that plays a critical role in regulating both innate and adaptive immune responses (Hayden and Ghosh 2004). NF-κB modulates inammatory response through the regulation of genes encoding pro-inammatory cytokines, adhesion molecules, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) (Barnes and Karin 1997, Chen et al. 1999, Baldwin 2001). Current approaches to the treatment of inammation rely on the inhibition of pro-inammatory mediator production. In particular, COX-2, the key inducible enzyme responsible for producing prostanoids, and NF-κB can be attractive targets for developing anti-inammatory medicines. Nonsteroidal anti-inammatory drugs (NSAIDs) are among the most widely prescribed drug for the treatment
16.1 Acute and Chronic Inammation ......................................................................................... 215 16.2 Effect of Chitin on Inammation ......................................................................................... 216 16.3 Effect of Chitosan on Inammation ..................................................................................... 217 16.4 Effect of Chitin Derivatives on Inammation ...................................................................... 218 16.5 Effect of Chitosan Derivatives on Inammation .................................................................. 218 16.6 Effect of Glucosamine and Its Derivatives on Inammation ............................................... 219 16.7 Conclusions ...........................................................................................................................220 References ......................................................................................................................................220
of many inammatory diseases. However, their major disadvantage is the high incidence of gastric, renal, and hepatic adverse effects caused by the inhibition of prostaglandin (PG) synthesis. In recent years, anti-inammatory agents have been focused on selective inhibitors of COX-2 without inuencing the activity of constitutive COX-1 (Donnelly and Hawkey 1997). In recent years, it has been reported that chronic inammation is associated with an increased risk of malignant transformation. Phagocytic leukocytes in chronic inammatory process produce large amounts of reactive metabolites of oxygen and nitrogen that induce oxidative stress and lead to the oxidation of fatty acids and proteins in cell membranes, thus impairing their normal function. Moreover, DNA mutation indirectly induced by these reactive intermediates can be a major cause of malignant transformation and age-related diseases. In another aspect, inammation is involved in wound healing progression, which triggers the recruitment of leukocytes into skin injury. Neutrophils penetrate from local blood vessels into endothelia, and monocytes migrate from blood into tissues and differentiate into macrophages that secrete cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1β, and interleukin-6 regulate the immune responses, further recruiting immune cells to the site of infection. In addition, COX-2, one of the enzymes responsible for the production of PG, mediates the inammatory response. COX-2 inhibition might decrease scar collagen deposition after cutaneous injury (Willoughby and Tomlinson 1999). Transforming growth factors-β are also secreted by platelets, broblasts, and macrophages within the injury and are thought to act as attractants or inhibitors of keratinocyte, broblast, and inammatory cell migration, in the upregulation of collagen synthesis and the modulation of matrix turnover via effects on MMPs and their inhibitors (Witte 1998).
