Ameneh Ghaffarinia1, Cyrus Jalili2, Ali Mostafaie3, Shahram Parvaneh4, Nafiseh Pakravan5. 1. Dept. of Immunology, Medical School, Kermanshah University of Medical Sciences , Kermanshah, Iran. 2. Dept. of Anatomy, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran. 3. Dept. of Immunology, Medical School, Kermanshah University of Medical Sciences , Kermanshah, Iran ; Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. 4. Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. 5. Dept. of Microbiology & Immunology, Medical School, Alborz University of Medical Sciences, Karaj, Iran.
Abstract
BACKGROUND AND OBJECTIVES: Multiple sclerosis is an inflammatory disease of the central nervous system. This is due to migration of peripherally activated lymphocytes to central nervous system leading to inflammatory lesions. However, liver has an anti-inflammatory microenvironment. Myelin expression in the liver of transgenic mice suppresses inflammatory lesions within central nervous system. Considering the notion that the inflammatory events originate from periphery, we investigated if the liver was affected in an animal model for multiple sclerosis. METHODS: Experimental autoimmune encephalomyelitis was induced in male Lewis rats using guinea pig spinal cord and complete Freund's adjuvant. Weight, clinical score, and survival rate were evaluated for 14 days post immunization. Liver sections were taken and stained with Hematoxylin and Eosin and examined with an Olympus microscope. RESULTS: Mortality was accompanied by liver damage. Sinusoidal congestion, pycnotic nuclei within hepatocytes, hepatocyte necrosis, and severe widespread congestion along with fat accumulation within hepatocytes (fatty degeneration) were observed in liver tissue sections. CONCLUSION: Liver damage occurs in experimental autoimmune encephalomyelitis. The perpetuation of self antigen leading to continuous migration of extrahepatically activated T cells makes an inflammatory milieu in the liver. It follows migration and development of more inflammatory cells and may paralyses tolerance inducing mechanisms. Apart from central nervous system lesion, liver injury may act as synergistic factor for debilitation and mortality.
BACKGROUND AND OBJECTIVES:Multiple sclerosis is an inflammatory disease of the central nervous system. This is due to migration of peripherally activated lymphocytes to central nervous system leading to inflammatory lesions. However, liver has an anti-inflammatory microenvironment. Myelin expression in the liver of transgenic mice suppresses inflammatory lesions within central nervous system. Considering the notion that the inflammatory events originate from periphery, we investigated if the liver was affected in an animal model for multiple sclerosis. METHODS: Experimental autoimmune encephalomyelitis was induced in male Lewis rats using guinea pig spinal cord and complete Freund's adjuvant. Weight, clinical score, and survival rate were evaluated for 14 days post immunization. Liver sections were taken and stained with Hematoxylin and Eosin and examined with an Olympus microscope. RESULTS: Mortality was accompanied by liver damage. Sinusoidal congestion, pycnotic nuclei within hepatocytes, hepatocyte necrosis, and severe widespread congestion along with fat accumulation within hepatocytes (fatty degeneration) were observed in liver tissue sections. CONCLUSION:Liver damage occurs in experimental autoimmune encephalomyelitis. The perpetuation of self antigen leading to continuous migration of extrahepatically activated T cells makes an inflammatory milieu in the liver. It follows migration and development of more inflammatory cells and may paralyses tolerance inducing mechanisms. Apart from central nervous system lesion, liver injury may act as synergistic factor for debilitation and mortality.
Entities:
Keywords:
Experimental Autoimmune Encephalomyelitis; Lewis Rat; Liver Damage; Mortality
Authors: P A Knolle; G Gerken; E Loser; H P Dienes; F Gantner; G Tiegs; K H Meyer zum Buschenfelde; A W Lohse Journal: Hepatology Date: 1996-10 Impact factor: 17.425
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