The route of enteric infection in normal mice.
The route of enteric infection in normal mice.
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DOI：
10.1084/jem.139.5.1189
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发表时间：
1974-05-01
期刊：
影响因子：
--
通讯作者：
Collins FM
中科院分区：
文献类型：
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作者：
Carter PB;Collins FM
本研究追踪了口服小鼠伤寒的早期发病机制。经肠内注射的肠炎沙门氏菌在正常的未受干扰的肠道中迅速移动，因此在最初的几个小时后，盲肠和大肠中只留下一小部分残留物。肠壁的染料注射被用来显示来自胃肠道离散部分的淋巴可能通过局部的Peyer’s斑块流入单独的淋巴结。电镀技术能够在不同的佩耶氏斑块和引流淋巴结中检测到肠炎沙门氏菌的单个集落形成单位，这表明，尽管盲肠和大肠暴露于大量沙门氏菌的时间比小肠长，但细菌渗透的主要部位涉及远端回肠。小肠和盲肠的这一区域均由远端肠系膜淋巴结排出，是感染后24小时内唯一含有可检测到的活沙门氏菌的淋巴结。幽门淋巴结、肠系膜近端淋巴结（引流胃和十二指肠）、胰腺淋巴结和尾端淋巴结（引流横结肠和降结肠）都不含活的沙门氏菌。观察到沙门氏菌感染回肠黏膜及其Peyer's补丁。随着时间的推移，这种感染进展到引流淋巴结，最终到达肝脏和脾脏。本文讨论了这些发现与肠道疾病获得性耐药发展相关的一些含义。
This study followed the early pathogenesis of orally induced murine typhoid fever. Intragastrically administered Salmonella enteritidis moves quickly through the normal undisturbed gut so that only a small residuum remains in the cecum and large intestine after the first few hours. Dye injection of the gut wall was used to show that lymph from discrete portions of the gastrointestinal tract drains to separate lymph nodes, probably via the regional Peyer's patches. Plating techniques capable of detecting a single colony-forming unit of S. enteritidis within the different Peyer's patches and draining lymph nodes indicate that, although the cecum and large intestine are exposed to large numbers of Salmonella for longer time periods than the small intestine, the primary site of bacterial penetration involves the distal ileum. This area of the small intestine as well as the cecum are both drained by the distal mesenteric lymph nodes, and were the only nodes which contained detectable numbers of viable Salmonella over the first 24 h of infection. Neither the pyloric nor the proximal mesenteric lymph nodes (which drain the stomach and duodenum) nor the pancreatic and caudal lymph nodes (which drain the transverse and descending colon) contained viable Salmonella. Salmonella were observed to infect the ileal mucosa and its Peyer's patches. With time, this infection progresses to the draining lymph node and ultimately reaches the liver and spleen. Some of the implications of these findings relative to the development of acquired resistance to enteric disease are discussed.