Animal Morphophysiology Laboratory, Department of Biological and Environmental Sciences, São Paulo State University (UNESP), São Vicente, 11.380-97, Brazil.
Laboratory of Pathology and Infectious Diseases, Department of Pathology, FMUSP, São Paulo, 01246903, Brazil.
Exp Parasitol. 2022 Aug;239:108315. doi: 10.1016/j.exppara.2022.108315. Epub 2022 Jul 1.
Visceral leishmaniasis is a neglected tropical disease caused by parasites belonging to the Leishmania genus that infect macrophages in different tissues such as the spleen, liver, lymph nodes, bone marrow, and intestine. Therefore, this study aimed to investigate the integrity of the intestinal tract and the nitrergic (NADPH-dp) and metabolically active (NADH-dp) myenteric neurons of the duodenum of golden hamsters infected with L. (L.) infantum. Therefore, thirty golden hamsters were divided into six groups (n = 5); three of them were infected with 2 × 10 promastigote forms of L. (L.) infantum by intraperitoneal route (Infected Group - IG) and three were inoculated with saline solution (control group - CG). After 30, 60 and 90 days post-infection (DPI) infected animals were euthanized and the liver, spleen and duodenum were collected to analyze tissue parasitism. The duodenum was processed using usual histological techniques to analyze the main changes that occurred during infection and histochemical techniques to phenotype myenteric neurons. Amastigote forms were observed in the spleen, liver, and duodenum during all experimental periods, and tissue parasitism in these organs increased significantly over time. At 30 DPI, reduction in muscle tunic, increase in the total intestinal wall and the number of goblet cells PAS+ was observed. At 60 DPI, an increase in intestinal crypts and intraepithelial lymphocytes was observed, and a reduction in intestinal villi was observed at 90 DPI, along with an increase in crypt size. Regarding neurons, an increase in the density of the NADPH-dp population was observed at 30 DPI, but at 60 and 90 DPI a significant reduction of this population was observed. In general, infection progression was observed to cause significant morphofunctional changes in the duodenum of infected hamsters.
内脏利什曼病是一种被忽视的热带病,由属于利什曼属的寄生虫引起,这些寄生虫感染脾脏、肝脏、淋巴结、骨髓和肠道等不同组织中的巨噬细胞。因此,本研究旨在研究感染 L.(L.)婴儿利什曼原虫的金黄地鼠十二指肠的肠道完整性和氮能(NADPH-dp)和代谢活跃(NADH-dp)肌间神经元。因此,将 30 只金黄地鼠分为六组(n=5);其中三组通过腹腔途径感染 2×10 个前鞭毛体形式的 L.(L.)婴儿利什曼原虫(感染组 - IG),三组接种生理盐水(对照组 - CG)。感染后 30、60 和 90 天(DPI),处死感染动物,采集肝脏、脾脏和十二指肠进行组织寄生虫分析。十二指肠采用常规组织学技术处理,分析感染过程中发生的主要变化,并采用组织化学技术表型化肌间神经元。在所有实验期间均在脾脏、肝脏和十二指肠中观察到无鞭毛体形式,并且这些器官中的组织寄生虫随着时间的推移显著增加。在 30 DPI 时,观察到肌层减少,总肠壁和 PAS+杯状细胞数量增加。在 60 DPI 时,观察到肠隐窝和上皮内淋巴细胞增加,在 90 DPI 时观察到肠绒毛减少,同时隐窝大小增加。关于神经元,在 30 DPI 时观察到 NADPH-dp 群体密度增加,但在 60 和 90 DPI 时观察到该群体显著减少。总的来说,感染进展导致感染金黄地鼠十二指肠发生显著的形态功能变化。