Kupffer cell-dependent hepatitis occurs during influenza infection
Kupffer cell-dependent hepatitis occurs during influenza infection
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DOI：
10.2353/ajpath.2006.050875
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发表时间：
2006-04-01
影响因子：
6
通讯作者：
Pierce, RH
中科院分区：
文献类型：
--
作者：
Polakos, NK;Cornejo, JC;Pierce, RH
呼吸道感染，包括人类的流感，经常伴随着肝炎，这种肝炎通常是轻微的和自我限制的。这种肝损伤的机制还不是很清楚。在目前的研究中，我们表明流感相关性肝炎的发生是由于炎症灶的形成，其中包括凋亡的肝细胞、抗原特异性CD8(+)T细胞和Kupffer细胞。在继发性流感感染中，血清转氨酶水平升高，肝炎的组织学和血清酶标记物均升高，这与抗原特异性T细胞在发病机制中的主要作用一致。在肝脏中没有检测到病毒，这纯粹是肝脏“附带损害”的一个例子。值得注意的是，库普弗细胞的移除预防了肝炎。这种肝脏侧支损害可能是在许多肝外病毒感染过程中CD8(+)T细胞数量增加的普遍后果，对肝脏病理生物学产生重要影响。
Respiratory infections, including influenza in humans, are often accompanied by a hepatitis that is usually mild and self-limiting. The mechanism of this kind of liver damage is not well understood. in the present study, we show that influenza-associated hepatitis occurs due to the formation of inflammatory foci that include apoptotic hepatocytes, antigen-specific CD8(+) T cells, and Kupffer cells. Serum aminotransaminase levels were elevated, and both the histological and serum enzyme markers of hepatitis were increased in secondary influenza infection, consistent with a primary role for antigen-specific T cells in the pathogenesis. No virus could be detected in the liver, making this a pure example of "collateral damage" of the liver. Notably, removal of the Kupffer cells prevented the hepatitis. Such hepatic collateral damage may be a general consequence of expanding CD8(+) T-cell populations during many extrahepatic viral infections, yielding important implications for liver pathobiology.