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急性肝坏死小鼠中 IgA+ 浆细胞和 IgA 表达降低。

Decreased IgA+ plasma cells and IgA expression in acute liver necrosis mice.

机构信息

Department of Infectious Diseases, The First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning Province, China.

出版信息

World J Gastroenterol. 2010 Aug 14;16(30):3827-33. doi: 10.3748/wjg.v16.i30.3827.

Abstract

AIM

To investigate the number of intestinal immunoglobulin A (IgA+) plasma cells and expression of intestinal IgA in mice with acute liver necrosis.

METHODS

A model of acute liver necrosis was established by intraperitoneal injection of galactosamine (GalN) and lipopolysaccharide (LPS). Sixty mice were randomly divided into one of 4 equal groups: normal control, acute liver necrosis, LPS, or GalN. Hematoxylin and eosin staining, immunohistochemistry, and an enzyme-linked immunosorbent assay were employed to assess liver and intestinal injury, count intestinal IgA+ plasma cells, and measure the expression level of IgA and interferon gamma (IFN-gamma) in the small intestinal mucosa of mice.

RESULTS

Injured intestinal mucosa was observed in the acute liver necrosis group but not in the normal, LPS or GalN groups. Compared with the normal group, intestinal IgA+ plasma cells were slightly decreased in the LPS and GalN groups [429 +/- 20 per high power field (HPF), 406 +/- 18/HPF, respectively], whereas they were markedly decreased in the acute liver necrosis group (282 +/- 17/HPF vs 495 +/- 26/HPF in normal group, P < 0.05). The expression of intestinal IgA was also slightly decreased in LPS and GalN groups, but was markedly reduced in the acute liver necrosis group as determined by enzyme-linked immunosorbent assay (P < 0.05). In contrast, the level of IFN-gamma was slightly increased in LPS, GalN and acute liver necrosis groups, but with no statistical significance (P > 0.05).

CONCLUSION

Intestinal IgA+ plasma cells and IgA expression levels indicating that mucosal immune barrier dysfunction, does exist in acute liver necrosis.

摘要

目的

研究急性肝坏死小鼠肠道免疫球蛋白 A(IgA)+浆细胞数量和肠道 IgA 的表达。

方法

采用腹腔注射半乳糖胺(GalN)和脂多糖(LPS)建立急性肝坏死模型。将 60 只小鼠随机分为正常对照组、急性肝坏死组、LPS 组和 GalN 组,每组 15 只。采用苏木精-伊红染色、免疫组化和酶联免疫吸附试验检测肝肠损伤,计数肠道 IgA+浆细胞,并检测小鼠小肠黏膜 IgA 和干扰素γ(IFN-γ)的表达水平。

结果

急性肝坏死组小鼠损伤的肠黏膜,而正常组、LPS 组和 GalN 组未观察到这种情况。与正常组相比,LPS 组和 GalN 组肠道 IgA+浆细胞略有减少[分别为 429 ± 20 个/高倍视野(HPF)、406 ± 18/HPF],而急性肝坏死组则明显减少(282 ± 17/HPF 比正常组 495 ± 26/HPF,P < 0.05)。LPS 组和 GalN 组肠道 IgA 的表达也略有减少,但急性肝坏死组明显减少(酶联免疫吸附试验检测,P < 0.05)。相反,LPS、GalN 和急性肝坏死组 IFN-γ 水平略有升高,但无统计学意义(P > 0.05)。

结论

急性肝坏死时存在黏膜免疫屏障功能障碍,表现为肠道 IgA+浆细胞和 IgA 表达水平降低。

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