Gebert Andreas, Steinmetz Ivo, Fassbender Susanne, Wendlandt Karl-Heinz
Institute of Anatomy, University of Lübeck, Lübeck, Germany.
Am J Pathol. 2004 Jan;164(1):65-72. doi: 10.1016/S0002-9440(10)63097-0.
Membranous (M) cells are specialized epithelial cells of the Peyer's patches that sample antigens from the gut lumen, thereby enabling the host to respond immunologically. Recent studies suggest that this transport can be up-regulated within hours by de novo formation of M cells from enterocytes. To test this hypothesis, we used an in vivo model and induced the transcytosis of tracers in Peyer's patches by application of Streptococcus pneumoniae R36a into the gut lumen. Using cell-type-specific markers, we quantified M cells in the Peyer's patch domes, lymphocytes associated with M cells, and the transport rate for experimentally applied microbeads after 3 hours of exposure to R36a. The transport of latex microbeads was significantly increased by +131% in the R36a-treated patches as compared to buffer controls (P < 0.001). While in controls, each M cell was associated with 2.05 +/- 0.64 lymphocytes, a significant increase (+55.1%; P < 0.001) was determined in the R36a-treated patches. However, no statistical difference was detected in the percentage of M cells in the dome epithelia (46.0 +/- 4.6% versus 45.5 +/- 3.8%). It is concluded that bacteria-induced up-regulation of particle transport in Peyer's patch domes is due to an increased transport rate of the M cells, but not to a de novo formation of M cells. The data support the hypothesis that M cells represent a separate cell lineage that does not derive from enterocytes on the domes.
膜性(M)细胞是派尔集合淋巴结中的特化上皮细胞,可从肠腔中摄取抗原,从而使宿主能够产生免疫反应。最近的研究表明,通过肠上皮细胞重新形成M细胞,这种转运可在数小时内上调。为了验证这一假设,我们使用了一种体内模型,并通过将肺炎链球菌R36a应用于肠腔来诱导派尔集合淋巴结中示踪剂的转胞吞作用。使用细胞类型特异性标记物,我们对派尔集合淋巴结圆顶中的M细胞、与M细胞相关的淋巴细胞以及暴露于R36a 3小时后实验应用微珠的转运速率进行了定量。与缓冲液对照组相比,R36a处理的圆顶中乳胶微珠的转运显著增加了131%(P < 0.001)。在对照组中,每个M细胞与2.05±0.64个淋巴细胞相关,而在R36a处理的圆顶中,这一数量显著增加(+55.1%;P < 0.001)。然而,在圆顶上皮中M细胞的百分比方面未检测到统计学差异(46.0±4.6%对45.5±3.8%)。结论是,细菌诱导的派尔集合淋巴结圆顶中颗粒转运的上调是由于M细胞转运速率的增加,而不是M细胞的重新形成。这些数据支持了M细胞代表一个独立的细胞谱系且并非源自圆顶上的肠上皮细胞这一假设。