1.Clinical and pathological characteristics and pathogenesis of autoimmune hepatitis.
Jingmin ZHAO ; Songshan WANG ; Yanling SUN ; Guangde ZHOU ; Ping LIU ; Erhong MENG ; Shaojie XIN ; Taihe ZHANG ; Fusheng WANG ; Yuanli MAO ; Li LI ; Yingxin LI ; Hongfei ZHANG ; Lingxia ZHANG ; Jumei CHEN
Chinese Journal of Experimental and Clinical Virology 2002;16(1):27-30
BACKGROUNDTo explore the clinical and pathological characteristics and pathogenesis of autoimmunohepatitis (AIH).
METHODSThe serum and liver biopsy specimens and clinical data of 26 cases with patients with AIH were analyzed and scored according to the criteria of International autoimmune hepatitis (IAIHG, 1999). The changes of dendritic cells (DC) in the liver tissues were observed with a panel of DC markers (CD-80/B7-1, CD-86/B7-2, CD-1a and HLA-DR) and immunohistochemistry, and the activation of hepatic stellate cells (HSC) and the expression of TGF-alpha were also detected. Liver tissue specimens from 10 patients with chronic viral hepatitis B and C respectively and 5 normal liver specimens were chosen as controls.
RESULTSMean aggregate scores of 26 AIH cases, including 21 cases of type B (80.8%) and 5 cases of type C (19.2%), which were 18.6 +/- 1.4 and 19.1 +/- 2.1 respectively. There were significant differences between the type B and type C in the average age levels of serum ALT and AST, and alpha-Glo (P <0.001 or P< 0.01 or P <0.05). Histological features of all the AIH liver tissues showed the lesions of chronic active hepatitis such as interface hepatitis/piecemeal necrosis (100%), obvious lobular inflammation (type B 95.2%, type C 100%), bridging necrosis (57.1% type B, 80.0% type C, P<0.05), rosetting of liver cells (71.4% type B, 100% type C, P<0.01), central lobular confluent necrosis (33.3% type B, 80.0% type C, P<0.001), predominant plasmacytic infiltration (type B 95.2%, type C 20.0%, P<0.001). The rates of increased and concentrated DC in the portal and lobular areas, especially in the active lesions in type B and type C AIH were 85.7% (18/21) and 5/5 respectively. It was found that DC and lymphocytes surrounded the hepatocytes which partly expressed HLA-DR antigen, while there were no or a few HLA-DR positive hepatocytes in controls. Meanwhile, the number of alpha-SMA positive HSC and the expression of TGF- were obviously increased in AIH liver tissues.
CONCLUSIONSSeveral clinical and pathological features of AIH were identified in this study. As an antigen-presenting cell, DC might play an important role in the pathogenesis of AIH. In China, sub-type B of AIH might be more frequent than sub-type C and there were differences in clinical aspects, serology and pathology between the two types.
Adolescent ; Adult ; Child ; Dendritic Cells ; immunology ; Female ; Hepatitis, Autoimmune ; blood ; pathology ; Humans ; Liver ; pathology ; Male ; Middle Aged
2.The change in apoptosis and proliferation of pulmonary tissue cells in rats with smoke inhalation injury.
Wenjun LI ; Zongcheng YANG ; Xiaodong YANG ; Tianpeng JI ; Hong ZHANG ; Erhong LI ; Guanghe ZHAO ; Bin ZHANG ; Xia LIU
Chinese Journal of Burns 2002;18(3):139-141
OBJECTIVETo observe the rule of the change of apoptosis and proliferation of pulmonary tissue cells in rats with inhalation injury, so as to explore the significance of apoptosis in the repairing process of pulmonary tissue injury.
METHODSSmoke inhalation injury model was established in rats. The rats were randomly divided into normal control (NC) and smoke inhalation injury (SI) groups. TUNEL and immunohistochemistry methods were employed to determine the changes in cellular apoptotic and proliferating cell nuclear antigen (PCNA) indices of the pulmonary tissue at different postburn time points.
RESULTS(1) The apoptotic index increased at 2 postburn hours (PBHs) and remained at high levels thereafter. (2) The PCNA index increased at 12 PBHs, reaching top level at 3 postburn days (PBDs), remaining kept at relativly high level later.
CONCLUSIONApoptosis not only played roles in the early pulmonary injury after smoke inhalation injury, but also participated in the repair and modification of the proliferated tissue during later reconstruction.
Animals ; Apoptosis ; Cell Division ; Disease Models, Animal ; Female ; Lung ; pathology ; Male ; Proliferating Cell Nuclear Antigen ; metabolism ; Rats ; Rats, Wistar ; Smoke Inhalation Injury ; metabolism ; pathology