Inflammation could be defined as a means by which body tissues respond to all kinds of injuries (Roitt, 1997). It is a defense mechanism against infections caused by injuries. Physical stimuli such as a change in temperature, UV radiation or skin irritation can cause the release of inflammatory mediators such as cytokines which provide adequate defense of the immune system, chemokines which bring leukocytes to the site of inflammation , eicosanoids, neuropeptides, etc. acute or chronic. Acute inflammation is an immediate response to trauma; in which the body fights against foreign bodies and heals wounds. Inflammatory mediators are released by the cell, causing an immune response. Vasolidation is another stage of acute inflammation; it causes an increase in blood flow and thus increases the permeability of blood vessels, which then results in the release of plasma proteins into the affected tissues (Spector & Willoughby, 1963). This could be characterized by redness, swelling and increased heat in the affected area. After vasolidation, inflammatory cells enter the injured tissue due to increased permeability. Mast cells are responsible for the release of mediators like cytokines and chemokines that eliminate dead cells and toxins. This is followed by the release of other important mediators from the endothelial cells. In order to make the inflammatory response effective, leukocytes, other mediators such as leukotrienes and kinins. The chemokine brings leukocytes to the site of inflammation, plasma proteins capable of destroying pathogens are initiated, the injury begins to heal, and then acute inflammation ceases. Under normal conditions, the inflammatory response is turned off by anti-inflammatory mechanisms to prevent...... middle of article......NJ & Gibson, RM (2006).The role of inflammation in CNS injuries and diseases. The British Journal of Pharmacology. 1 Inflammation in multiple sclerosis: the good, the bad and the complex47, S232–S240.Martino, G., Furlan, R. & Poliani, PL The pathogenic role of inflammation in multiple sclerosis. Reverend Neurol. June 16-30, 2000; 30(12):1213-7.Rooks, A. & Burns, T. (2010). Rook's textbook of dermatology. Vol 4 (Chapter 12). John Wiley and Sons. Roitt, I. M. (1997). Essential Immunology (Ninth Edition). Blackwell Scientific, Oxford. Spector, W. G. and D. A. Willoughby (1963). Inflammatory responses. J. Pathol. Bacterium. 27: 118-149. Martino, G., Adorini, L., Rieckmann, P., Hillert, J. Kallmann, B. Comi, G. & Filippi, M. Inflammation in multiple sclerosis: the good, the bad and the complex. Neurology from the Lancet. Volume 1, number 8, December 2002, pages 499-509