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首页> 外文期刊>Comparative Medicine >Histologic, cytologic, and bacteriologic examinations of experimentally induced Salmonella typhimurium infection in lewis rats
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Histologic, cytologic, and bacteriologic examinations of experimentally induced Salmonella typhimurium infection in lewis rats

机译：刘易斯大鼠实验性鼠伤寒沙门氏菌感染的组织学，细胞学和细菌学检查

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Background and Purpose: Histopathologic changes, cellular composition, and bacterial spreading were studied in rat spleen after experimentally induced infection with Salmonella typhimurium. Methods: Lewis rats were inoculated intraperitoneally with10~6 bacteria. Spleen weight, cell numbers, and cell surface markers were studied together with histopathologic changes, and expression of inducible nitric oxide synthase (iNOS). The spread of bacteria to blood, spleen ,liver, mesenteric lymph nodes, lung, and kidney was studied at 12 hours, and 1, 3, 7, 14, and 28 days after inoculation. Results: Experimentally induced infection caused an increase in spleen weight and leukocyte numbers, and a decrease in CD49d, on postinoculation days (PID) 3 through 7. Numerous granulomas were disseminated throughout the splenic red pulp also on PID 3 through 7. From PID 14 on, clearance of cellular exudate and regeneration of tissue structure were observed. Massive expression of iNOS was seen on PID 3. Bacterial growth was observed in liver and spleen from 12 hours to 14 days after inoculation. Bacteria were detected in blood on PID 3 and mesenteric lymph nodes were infected from PID 3 through 14. Conclusions: Salmonella typhimurium was rapidly taken up by the reticuloendothelial system. The infection induced weight increase and reversible changes in the spleen, peaking on PID 3 with granuloma formation and infiltration with macrophages. On PID 3, extensive production of iNOS within the granulomas was observed, suggesting initial killing of phagocytosed bacteria, followed by bacterial clearance and tissue regeneration. Cell surface marker expression on CD4~+ T cells indicated no change in their numbers; however, there was a time-dependent change in expression ofCD49d.
机译：背景与目的：研究鼠伤寒沙门氏菌感染后大鼠脾脏的组织病理学变化，细胞组成和细菌传播。方法：Lewis大鼠腹腔接种10〜6种细菌。研究了脾脏重量，细胞数量和细胞表面标志物，以及组织病理学变化和诱导型一氧化氮合酶（iNOS）的表达。在接种后12小时以及1、3、7、14和28天研究了细菌在血液，脾脏，肝脏，肠系膜淋巴结，肺和肾脏中的传播。结果：实验诱导的感染在接种后第3天到第7天导致脾脏重量和白细胞数量增加，而CD49d减少。在脾脏红髓中，在PID 3到7上也散布了许多肉芽肿。从PID 14之后，观察到细胞渗出液的清除和组织结构的再生。在PID 3上可见iNOS的大量表达。接种后12小时到14天，肝脏和脾脏中细菌生长。在PID 3的血液中检测到细菌，并从PID 3到14感染了肠系膜淋巴结。结论：鼠伤寒沙门氏菌被网状内皮系统迅速吸收。感染引起的体重增加和脾脏的可逆变化，在PID 3上达到峰值，并伴有肉芽肿形成和巨噬细胞浸润。在PID 3上，观察到肉芽肿中iNOS的大量产生，这表明吞噬细胞的细菌最初被杀死，随后细菌清除和组织再生。 CD4〜+ T细胞表面细胞标志物表达无变化。但是，CD49d的表达随时间变化。

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