目的 探讨半乳糖凝集素与受体的相互作用对弓形虫感染小鼠小肠免疫病理的调节作用。方法 将18只雌性BALB/c小鼠随机分成4组：未感染组（naive组）4只、α-乳糖组（lactose组）4只、弓形虫感染组（Tg组）5只和弓形虫感染+lactose组（Tg+lactose组）5只。Tg组和Tg+lactose组每鼠腹腔注射约1 000个弓形虫速殖子，naive组和lactose组腹腔注射PBS 0.2 ml。感染后当天开始，Tg+lactose组和lactose组每鼠腹腔注射0.2 mol/L的lactose 0.2 ml，naive组和Tg组每鼠腹腔注射等体积的PBS，早、晚各1次，连续注射7 d。感染弓形虫后，记录各组小鼠的生存时间。在感染后第7天处死小鼠，取空肠中段进行石蜡切片和HE染色，观察小鼠小肠组织的病理变化；取小鼠空肠下段提总RNA后逆转录，以β肌动蛋白（β-actin）作为内参基因，qRT-PCR检测小鼠小肠组织弓形虫表面抗原1（SAG1）、半乳糖凝集素3（galectin-3）、galectin-9、T细胞免疫球蛋白黏蛋白-3（Tim-3）、白细胞分化抗原137（CD137）、白细胞介素12（IL-12）、γ-干扰素（IFN-γ）、IL-10、IL-4、转化生长因子β（TGF-β）、趋化因子受体2（CCR2）、和几丁质酶3样分子3（Ym1）的mRNA相对表达水平。结果 感染弓形虫后，naive组和lactose组小鼠无死亡，Tg组小鼠的存活时间为182~188 h，Tg+lactose组小鼠的存活时间为180~182 h；两组小鼠的生存时间差异有统计学意义（χ² = 19.52，P < 0.05）。HE染色结果显示，naive组和lactose组小鼠的空肠组织未观察到炎症改变；Tg组和Tg+lactose组小鼠的小肠组织观察到肠绒毛缩短，肠隐窝变浅，绒毛顶端上皮细胞坏死，小肠黏膜组织中有炎症细胞浸润。与Tg组的相比，Tg+lactose组小鼠小肠组织的病理损伤更加严重。qRT-PCR结果显示，Tg+lactose组小鼠小肠组织SAG1的mRNA相对表达水平为9.17 ± 1.65，高于Tg组的1.00 ± 0.84（t = 4.40，P < 0.05）。naive组、lactose组、Tg组和Tg+lactose组小鼠小肠组织galectin-3的mRNA相对表达水平分别为1.00 ± 0.28、1.71 ± 0.31、2.46 ± 1.11和7.10 ± 1.57（F = 10.15，P < 0.01），galectin-9的mRNA相对表达水平分别为1.00 ± 0.31、1.44 ± 0.26、3.21 ± 1.01和7.00 ± 1.08（F = 14.53，P < 0.01），Tim-3的mRNA相对表达水平分别为1.00 ± 0.12、0.88 ± 0.28、1.64 ± 0.31和4.89 ± 0.69（F = 19.15，P < 0.01），CD137的mRNA相对表达水平分别为1.00 ± 0.42、1.03 ± 0.30、0.89 ± 0.11和3.84 ± 0.77（F = 8.46，P < 0.01），IL-12的mRNA相对表达水平分别为1.00 ± 0.35、1.14 ± 0.56、12.37 ± 4.43和18.42 ± 3.89（F = 10.18，P < 0.01），IFN-γ的mRNA相对表达水平分别为1.00 ± 0.56、1.65 ± 0.53、5.57 ± 1.84和21.26 ± 6.48（F = 10.38，P < 0.01），IL-10的mRNA相对表达水平分别为1.00 ± 0.20、1.10 ± 0.25、8.65 ± 2.52和21.98 ± 3.96（F = 20.84，P < 0.01）。小鼠小肠组织中IL-4、TGF-β和CCR2的mRNA相对表达水平在naive组、lactose组、Tg组和Tg+lactose组之间差异无统计学意义（F = 1.09、4.74、2.03，均P > 0.05）。naive组和lactose组未检测到Ym1的mRNA表达，Tg组和Tg+lactose组Ym1的mRNA相对表达水平差异无统计学意义（t = 0.24，P > 0.05）。结论 阻断半乳糖凝集素-受体相互作用后，弓形虫感染小鼠的小肠组织虫荷增加、病理损伤加重，galectin-3、galectin-9、Tim-3、CD137、IL-10和IFN-γ的表达上调。

Objective To investigate the regulatory effect of galectin-receptor interaction on the small intestine immunopathology of Toxoplasma gondii-infected mice. Methods Eighteen female BALB/c mice were randomly divided into 4 groups: 4 mice in uninfected group (naive group), 4 mice in lactose group (lactose group), 5 mice in T. gondii infection group (Tg group) and 5 mice in T. gondii infection + lactose group (Tg+lactose group). Each mouse in the Tg group and the Tg+lactose group was intraperitoneally (i.p.) injected with 1 000 tachyzoites of T. gondii RH strain, while the naive group and lactose group were i.p. injected with 0.2 ml PBS. Starting from day 0 post infection, each mouse in the Tg+lactose group and the lactose group was i.p. injected with 0.2 ml 0.2 mol/L of lactose, while each mouse in the naive group and the Tg group was i.p. injected with an equal volume of PBS, once in the morning and once in the evening for 7 consecutive days. After infection with T. gondii, the mice survival time in each group was recorded. The mice were euthanized on the 7th day after infection to collect middle segment of jejunum from each mouse for prepareing paraffin sections, which were stained with hematoxylin and eosin (HE) to observe the pathological changes; from the lower segment of jejunum of each mouse, total RNA was extracted and reverse-transcribed, and used in quantitative real-time reverse transcription PCR (qRT-PCR) with β-actin as an internal reference gene to detect the relative mRNA expression level of surface antigen 1 (SAG1), galectin-3, galectin-9, T cell immunoglobulin mucin 3 (Tim-3), leukocyte differentiation antigen 137 (CD137), interleukin 12 (IL-12), interferon-γ (IFN-γ), IL-10, IL-4, transforming growth factor β (TGF-β), chemokine receptor 2 (CCR2) and chitinase 3 like molecule 3 (Ym1). Results After infection with T. gondii, there was no mice died in the naive group and the lactose group. The survival time of the mice in the Tg group was 182-188 h, and the survival time of the mice in the Tg+lactose group was 180-182 h; the difference of the survival time between the two groups was statistically significant (χ² = 19.52, P < 0.05). HE staining showed no inflammation in the mice jejunal tissue in the naive group and lactose group. Shortened intestinal villus, shallower intestinal crypts, necrosis of epithelial cells at the top of villi and inflammatory cell infiltration in the intestinal mucosa were observed in the mice small intestine from the Tg group and Tg+lactose group. Compared with the Tg group, the pathological change of the mice small intestine in the Tg+lactose group was more severe. The qRT-PCR results showed that the relative mRNA expression of SAG1 in the mice small intestine of the Tg+lactose group was 9.17 ± 1.65, which was higher than that in the Tg group (1.00 ± 0.84, t = 4.40, P < 0.05). The relative mRNA expression levels of galectin-3 in the mce small intestine of the naive group, lactose group, Tg group, and Tg+lactose group were 1.00 ± 0.28, 1.71 ± 0.31, 2.46 ± 1.11, and 7.10 ± 1.57, respectively (F = 10.15, P < 0.01). The mRNA expression levels of galectin-9 in the 4 groups were 1.00 ± 0.31, 1.44 ± 0.26, 3.21 ± 1.01, and 7.00 ± 1.08, respectively (F = 14.53, P < 0.01). The mRNA expression levels of Tim-3 in the 4 groups were 1.00 ± 0.12, 0.88 ± 0.28, 1.64 ± 0.31, and 4.89 ± 0.69, respectively (F = 19.15, P < 0.01). The mRNA expression levels of CD137 in the 4 groups were 1.00 ± 0.42, 1.03 ± 0.30, 0.89 ± 0.11, and 3.84 ± 0.77, respectively (F = 8.46, P < 0.01). The mRNA expression levels of IL-12 in the 4 groups were 1.00 ± 0.35, 1.14 ± 0.56, 12.37 ± 4.43, and 18.42 ± 3.89, respectively (F = 10.18, P < 0.01). The mRNA expression levels of IFN-γ in the 4 groups were 1.00 ± 0.56, 1.65 ± 0.53, 5.57 ± 1.84, and 21.26 ± 6.48, respectively (F = 10.38, P < 0.01). The mRNA expression levels of IL-10 in the 4 groups were 1.00 ± 0.20, 1.10 ± 0.25, 8.65 ± 2.52, and 21.98 ± 3.96, respectively (F = 20.84, P < 0.01). The mRNA expression levels of IL-4, TGF-β, and CCR2 in the mice small intestine among the naive group, lactose group, Tg group, and Tg+lactose group had no statistically significant differences (F = 1.09, 4.74, and 2.03, P > 0.05). Ym1 mRNA expression was not detected in the naive group and lactose group, and Ym1 mRNA expression levels between the Tg group and the Tg+lactose group had no statistically significant difference (t = 0.24, P > 0.05). Conclusion Blockage of galectins-receptor interaction in mice infected with T. gondii leads to increased parasite burden in small intesting tissues, and aggravated pathological impairment, as well as upregulated expression of galectin-3, galectin-9, Tim-3, CD137, IL-10 and IFN-γ.