HISTOCHEMICAL LOCALIZATION OF ALKALINE AND ACID PHOSPHATASE AND THEIR PROBABLE ROLE IN GUINEA PIGS WITH EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
Dr. Mohamed Noorulla*
ABSTRACT
Experimental allergic encephalomyelitis has attracted wide attention as a meaningful model for probing the basis of autoimmune reactivity and defining its role in neurologic disorders characterized by inflammation and demyelination as in multiple sclerosis in man. Activated inflammatory cells and microglia can secrete a variety of enzymes and factors responsible for the breakdown of myelin in the autoimmune diseases like multiple sclerosis and experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis was induced in the adult healthy guinea pigs by weekly intradermal injections of homologous whole brain and spinal cord antigen together with complete Freund’s adjuvant into the foot pad of the animal. The animals were observed for clinical features of the disease after injection. Histochemical localization of alkaline phosphatase was carried out by Gomori’s Calcium-Cobalt method and acid phosphatase by Gomori’s Lead Acetate method. The increased activity of alkaline phosphatase indicates its involvement in active transport needed for the phagocytic action at the lesion site. The increased activity of acid phosphatase might be due to increased activity in the microgliocytes or phagocytes or hypertrophied astrocytes. Probably the inflammatory cells such as lymphocytes and monocytes may be the cause of the increased acid phosphatase activity in the central nervous system of animals with experimental allergic encephalomyelitis, and that enzymes from these cells possess the capability of digesting myelin basic protein.
Keywords: EAE, MS, Inflammation, Demyelination, Alkaline phosphatase, Acid phosphatase.
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