Ghaffarinia Ameneh, Jalili Cyrus, Mostafaie Ali, Parvaneh Shahram, Pakravan Nafiseh
Dept. of Immunology, Medical School, Kermanshah University of Medical Sciences , Kermanshah, Iran.
Dept. of Anatomy, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Iran J Pathol. 2015 Winter;10(1):9-16.
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.
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.
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.
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.
多发性硬化是一种中枢神经系统的炎症性疾病。这是由于外周激活的淋巴细胞迁移至中枢神经系统，导致炎症性病变。然而，肝脏具有抗炎微环境。转基因小鼠肝脏中的髓磷脂表达可抑制中枢神经系统内的炎症性病变。鉴于炎症事件起源于外周的观点，我们研究了在多发性硬化动物模型中肝脏是否受到影响。
使用豚鼠脊髓和完全弗氏佐剂在雄性Lewis大鼠中诱导实验性自身免疫性脑脊髓炎。在免疫后14天评估体重、临床评分和存活率。取肝脏切片，用苏木精和伊红染色，并用奥林巴斯显微镜检查。
死亡伴随着肝脏损伤。在肝脏组织切片中观察到窦状隙充血、肝细胞内固缩核、肝细胞坏死、严重广泛的充血以及肝细胞内脂肪堆积（脂肪变性）。
在实验性自身免疫性脑脊髓炎中会发生肝脏损伤。自身抗原的持续存在导致肝外激活的T细胞持续迁移，在肝脏中形成炎症环境。随之而来的是更多炎症细胞的迁移和发展，并可能使耐受诱导机制瘫痪。除了中枢神经系统病变外，肝脏损伤可能是导致衰弱和死亡的协同因素。
