目的 了解刚地弓形虫（以下简称弓形虫）急性感染对小鼠小肠黏膜免疫应答和免疫病理的影响及其机制。方法 将15只昆明小鼠随机分成感染组（10只）和对照组（5只）。感染组小鼠腹腔注射弓形虫RH株速殖子（1 × 10³个），对照组小鼠注射等量PBS。感染后第7天，取小鼠回肠后段2 cm和肠系膜淋巴结，进行石蜡包埋、切片和苏木素-伊红染色后，观察小肠和肠系膜淋巴结的病理变化，测量小肠绒毛长度和隐窝深度，计数杯状细胞和潘氏细胞数量；进行免疫组织化学染色，计数小肠组织中CD68阳性细胞数量。使用GraphPad Prism10.1.2软件对数据进行独立样本t检验。结果 对照组小鼠小肠绒毛和肠系膜淋巴结组织结构完整，形态正常。感染组小鼠小肠病理损伤严重，小肠绒毛上皮细胞坏死，肠绒毛脱落或缩短，肠隐窝变深，小肠黏膜组织中可见大量炎症细胞浸润；肠系膜淋巴结组织结构破坏，可见弥漫性坏死病灶，感染组小鼠小肠和肠系膜淋巴结组织中均可观察到弓形虫速殖子和假包囊。感染组小鼠小肠绒毛长度为（93.07 ± 2.158）μm，短于对照组的（125.0 ± 19.36）μm（t = 2.756，P < 0.05）；感染组小鼠的小肠隐窝深度为（49.04 ± 8.809）μm，深于对照组的（39.9 ± 4.174）μm（t = 2.382，P < 0.05）。感染组小鼠10根小肠绒毛中的杯状细胞数量为（78.70 ± 14.01）个，少于对照组的（96.71 ± 13.89）个（t = 2.618，P < 0.05）；感染组小鼠10个小肠隐窝中的杯状细胞数量为（31.60 ± 8.60）个，少于对照组的（53.17 ± 13.03）个（t = 4.014，P < 0.05）。感染组小鼠20个小肠隐窝中的潘氏细胞数量为（69.80 ± 8.90）个，少于对照组的（103.0 ± 4.86）个（t = 8.342，P < 0.01）。感染组小鼠小肠组织每个高倍视野下CD68⁺巨噬细胞数量为（42.33 ± 11.41）个，多于对照组的（15.75 ± 2.754）个（t = 4.496，P < 0.01）；感染组小鼠小肠派尔集合淋巴结组织每个高倍视野下CD68⁺巨噬细胞数量为（185.0 ± 23.80）个，多于对照组的（15.75 ± 2.754）个（t = 9.286，P < 0.01）。结论 弓形虫急性感染可诱导小鼠小肠损伤，小肠组织中的杯状细胞和潘氏细胞数量减少，CD68⁺巨噬细胞数量增加，提示杯状细胞、潘氏细胞和巨噬细胞可能参与小肠黏膜免疫应答和免疫病理。

Objective To examine the effect of acute Toxoplasma gondii infection on mucosal immune responses and immunopathology in mouse small intestines and unravel the mechanism. Methods Fifteen Kunming mice were randomly divided into two groups, including the T. gondii infection group (10 mice) and the control group (5 mice). Mice in the infection group were intraperitoneally injected with tachyzoites of the T. gondii RH strain (1 × 10³ tachyzoites per mouse), while animals in the control group were injected with an equal volume of PBS. Mice were sacrificed at 7 days post-infection, and the posterior section of small intestine (2 cm in length) and mesenteric lymph nodes were taken for paraffin embedding, preparing slices, and hematoxylin and eosin staining to observe the pathological changes of mice. The intestinal villi length and the crypt depth were measured, and the numbers of goblet cells and Paneth cells were counted. In addition, immunohistochemical staining was performed to count the number of CD68⁺ cells in small intestines. Differences of means were tested for statistical significance using independent sample t test with the software GraphPad Prism 10.1.2. Results The structures of mouse small intestinal villi and mesenteric lymph nodes were intact with a normal morphology in the control group, while mice in the infection group exhibited severe pathological damage in the small intestine, characterized by necrosis of villous epithelial cells, shedding or shortening of intestinal villi, deepening of intestinal crypts, and extensive infiltration of inflammatory cells in small intestinal mucosal tissues. Additionally, the histological structures of the mesenteric lymph nodes of mice in the infection group were disrupted, with diffuse necrotic lesions observed. T. gondii tachyzoites and pseudocysts were observed in mouse small intestines and mesenteric lymph nodes in the infection group. The mean length of mouse small intestinal villi was shorter in the infection group than that in the control group [(93.07 ± 2.158) μm vs. (125.0 ± 19.36) μm; t = 2.756, P < 0.05], and the mean depth of mouse small intestinal crypts was greater in the infection group than that in the control group [(49.04 ± 8.809) μm vs. (39.9 ± 4.174) μm; t = 2.382, P < 0.05]. The number of goblet cells per 10 mouse small intestinal villi was lower in the control group than that in the infection group [(78.70 ± 14.01) cells vs. (96.71 ± 13.89) cells; t = 2.618, P < 0.05], and the number of goblet cells per 10 mouse small intestinal crypts was fewer in the infection group than that in the control group [(31.60 ± 8.60) cells vs. (53.17 ± 13.03) cells; t = 4.014, P < 0.05]. The number of Paneth cells per 20 mouse small intestinal crypts was fewer in the infection group than that in the control group [(69.80 ± 8.90) cells vs. (103.0 ± 4.86) cells; t = 8.342, P < 0.01]. In addition, the number of CD68⁺ macrophages per high-power field in mouse small intestine tissue was larger in the infection group than that in the control group [(42.33 ± 11.41) cells vs. (15.75 ± 2.754) cells; t = 4.496, P < 0.01], and the number of CD68⁺ macrophages in mouse Peyer’s patches per high-power field was higher in the infection group than that in the control group [(185.0 ± 23.80) cells vs. (15.75 ± 2.754) cells; t = 9.286, P < 0.01]. Conclusion Acute T. gondii infection may induce small intestinal damage in mice, with a decrease in goblet cell and Paneth cell counts and an increase in CD68⁺ macrophage number in small intestinal tissues, suggesting that goblet cells, Paneth cells, and macrophages may contribute to mucosal immune responses and immunopathology of small intestines.