Biosciences and Physiopathology Program, State University of Maringá, Maringá, Brazil; Department of Basic Health Sciences, State University of Maringá, Maringá, Brazil.
Department of Clinical Analysis and Biomedicine, State University of Maringá, Maringá, Brazil; Department of Basic Health Sciences, State University of Maringá, Maringá, Brazil.
Tissue Cell. 2023 Oct;84:102194. doi: 10.1016/j.tice.2023.102194. Epub 2023 Aug 8.
Infection by Toxoplasma gondii may compromise the intestinal histoarchitecture through the tissue reaction triggered by the parasite. Thus, this study evaluated whether treatment with rosuvastatin modifies duodenal changes caused by the chronic infection induced by cysts of T. gondii. For this, female Swiss mice were distributed into infected and treated group (ITG), infected group (IG), group treated with 40 mg/kg rosuvastatin (TG) and control group (CG). After 72 days of infection, the animals were euthanized, the duodenum was collected and processed for histopathological analysis. We observed an increase in immune cell infiltration in the IG, TG and ITG groups, with injury to the Brunner glands. The infection led to a reduction in collagen fibers and mast cells. Infected and treated animals showed an increase in collagen fibers, acidic mucin-producing goblet cells, intraepithelial lymphocytes and mast cells, in addition to the reduction of muscle, neutral mucin-producing and Paneth cells. While treatment with rosuvastatin alone led to increased muscle layer, proportion of neutral mucin-producing goblet cells, Paneth cells, and reduction of collagen fibers. These findings indicate that the infection and treatment caused changes in the homeostasis of the intestinal wall and treatment with rosuvastatin potentiated most parameters indicative of inflammation.
刚地弓形虫感染可能通过寄生虫引发的组织反应破坏肠道组织形态结构。因此，本研究评估了氯吡格雷治疗是否能改变由刚地弓形虫包囊引起的慢性感染引起的十二指肠变化。为此，将雌性瑞士小鼠分为感染和治疗组（ITG）、感染组（IG）、40mg/kg 氯吡格雷治疗组（TG）和对照组（CG）。感染 72 天后，处死动物，采集十二指肠进行组织病理学分析。我们观察到 IG、TG 和 ITG 组免疫细胞浸润增加，Brunner 腺损伤。感染导致胶原纤维和肥大细胞减少。感染和治疗组动物表现出胶原纤维、产生酸性黏蛋白的杯状细胞、上皮内淋巴细胞和肥大细胞增加，同时肌肉、中性黏蛋白产生细胞和潘氏细胞减少。而单独使用氯吡格雷治疗导致肌肉层增加、产生中性黏蛋白的杯状细胞、潘氏细胞比例增加和胶原纤维减少。这些发现表明，感染和治疗导致肠道壁稳态发生变化，而氯吡格雷治疗增强了大多数炎症指标。
