Involvement of myeloid dendritic cells in the development of gastric secondary lymphoid follicles in Helicobacter pylori-infected neonatally thymectomized BALB/c mice
Involvement of myeloid dendritic cells in the development of gastric secondary lymphoid follicles in Helicobacter pylori-infected neonatally thymectomized BALB/c mice
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DOI：
10.1128/iai.71.4.2153-2162.2003
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发表时间：
2003-04-01
影响因子：
3.1
通讯作者：
Chiba, T
中科院分区：
文献类型：
--
作者：
Nishi, T;Okazaki, K;Chiba, T
我们先前描述了幽门螺杆菌诱导的滤泡性胃炎的动物模型，在腹腔胸腺切除（nTx）小鼠。然而，目前尚不清楚胃中的抗原呈递树突状细胞（DC）是否在H. pylori感染的nTx小鼠。我们研究了DC子集的分布，使用这个模型，并检查他们的角色。为了鉴定淋巴样和髓样DC，将切片用抗CD 11 c（泛DC标记物）与抗CD 8 α（淋巴样DC标记物）或抗CD 11b（髓样DC标记物）组合染色，并用共聚焦显微镜检查。通过实时PCR和免疫组化分析巨噬细胞炎性蛋白3 α（MIP-3 α）的表达，其化学吸引未成熟的DC。用抗SK-Y28抗体染色滤泡树突细胞（FDC）。在未感染的nTx小鼠中，在固有层底部观察到少数髓样和淋巴样DC，而在H.在pylori感染的nTx小鼠中，整个固有层中髓样DC的流入增加。在感染组成员的胃中也观察到FDC染色。MIP-3 α基因表达在感染nTx组中上调，免疫组化分析显示MIP-3 α阳性上皮细胞。这些数据表明H. pylori感染上调胃上皮细胞MIP-3a基因表达，并诱导nTx小鼠胃粘膜固有层中髓样DC的流入。髓样DC和FDCs可能参与了H. pylori感染的nTx小鼠。
We previously described an animal model of Helicobacter pylori-induced follicular gastritis in neonatally thymectomized (nTx) mice. However, it is still not clear whether antigen-presenting dendritic cells (DCs) in the stomach have a role in the development of secondary follicles in H. pylori-infected nTx mice. We investigated the distribution of DC subsets using this model and examined their roles. To identify lymphoid and myeloid DCs, sections were stained with anti-CD11c (pan-DC marker) in combination with anti-CD8alpha (lymphoid DC marker) or anti-CD11b (myeloid DC marker) and were examined with a confocal microscope. Expression of macrophage inflammatory protein 3alpha (MIP-3alpha), which chemoattracts immature DCs, was analyzed by real-time PCR and immunohistochemistry. Follicular dendritic cells (FDCs) were stained with anti-SK-Y28 antibodies. In noninfected nTx mice, a few myeloid and lymphoid DCs were observed in the bottom portion of the lamina propria, whereas in H. pylori-infected nTx mice, there was an increased influx of myeloid DCs throughout the lamina propria. FDC staining was also observed in the stomachs of members of the infected group. MIP-3alpha gene expression was upregulated in the infected nTx group, and the immunohistochemistry analysis revealed MIP-3alpha-positive epithelial cells. These data suggest that H. pylori infection upregulates MIP-3a gene expression in gastric epithelial cells and induces an influx of myeloid DCs in the lamina propria of the gastric mucosa in nTx mice. Myeloid DCs and FDCs might contribute to the development of gastric secondary lymphoid follicles in H. pylori-infected nTx mice.