Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice.
Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice.
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新生儿免疫球蛋白（Ig）G (FcRn) Fc受体在调节宿主IgG水平和IgG跨极化上皮屏障转运中起核心作用。我们试图阐明FcRn在控制胃幽门螺杆菌感染中的作用。用C57BL/6J野生型或FcRn−/−小鼠感染海曼螺杆菌，观察其胃损伤、细菌负荷及血清和胃液中抗原特异性IgG水平。抗h。在野生型小鼠的胃液中观察到heimannii IgG，而在FcRn - / -小鼠中没有观察到。相比之下，在FcRn - / -小鼠中，淋巴滤泡和细菌负荷随着更深的胃上皮浸润而增加。C57BL/6J野生型或FcRn - / -小鼠也感染了幽门螺杆菌SS1，这些小鼠的胃细菌负荷和抗h。血清和胃液幽门螺杆菌IgG水平与海曼嗜血杆菌感染相似。我们的数据表明，FcRn可以在胃中功能性表达，参与IgG的胞吞作用，并阻止海曼氏嗜血杆菌的定植和相关的感染病理后果。
Neonatal Fc receptors for immunoglobulin (Ig)G (FcRn) assume a central role in regulating host IgG levels and IgG transport across polarized epithelial barriers. We have attempted to elucidate the contribution of FcRn in controlling Helicobacter infection in the stomach. C57BL/6J wild-type or FcRn−/− mice were infected with Helicobacter heilmannii, and gastric lesions, bacterial load and the levels of antigen-specific IgG in serum and gastric juice were analyzed. The elevated levels of anti-H. heimannii IgG in gastric juice were observed exclusively in wild-type mice but not in FcRn−/− mice. In contrast, an increase in lymphoid follicles and bacterial loads along with deeper gastric epithelium invasion were noted in FcRn−/− mice. C57BL/6J wild-type or FcRn−/− mice were also infected with Helicobacter pylori SS1, and the results of the bacterial load in stomachs of these mice and the anti-H. pylori IgG levels in serum and gastric juice were similar to those from H. heilmannii infection. Our data suggest that FcRn can be functionally expressed in the stomach, which is involved in transcytosis of IgG, and prevent colonization by H. heilmannii and the associated pathological consequences of infection.
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影响因子：
0.8
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Park, JH;Hong, JJ;Park, JH
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Park, JH
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Claypool, SM;Dickinson, BL;Blumberg, RS
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Blumberg, RS
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3.4
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Francavilla, A
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Katsuyama, T