目的/背景肠易激综合征的发病机制包括多种因素,包括异常的胃肠蠕动,内脏敏感性增强,脑-肠轴功能障碍,心理影响,和肠道菌群的紊乱。这些因素主要表现为持续性或间歇性腹痛,腹泻,排便习惯的改变,或粪便特征的变化。在我们的调查中,我们深入研究了感染后肠易激综合征患者的机械屏障损伤和免疫功能障碍对症状的影响.方法选取20名健康对照者和49例肠易激综合征患者。在肠易激综合征患者中,我们根据ROMEIV诊断标准将其分为两组:感染后肠易激综合征组(n=23)和非感染后肠易激综合征组(n=26).为了比较临床特征,我们使用了胃肠道症状评定量表,抑郁自评量表,和焦虑自评量表。此外,我们采用了各种技术,包括苏木精和伊红(HE)染色,电子显微镜,酶联免疫吸附测定,和流式细胞术来评估免疫细胞的变化,免疫因子,炎症生物标志物,肠屏障功能。结果苏木精和伊红染色,与对照组相比,感染后肠易激综合征患者的中性粒细胞和浆细胞增加。此外,电子显微镜显示感染后肠易激综合征患者的超微结构变化,例如肠粘膜上皮细胞间隙扩大。相对而言,胃肠道症状评定量表,焦虑自评量表,与对照组和非感染后肠易激综合征组相比,感染后肠易激综合征组的抑郁自评量表评分显着升高(p<0.05)。此外,感染后肠易激综合征患者的中性粒细胞与淋巴细胞比率明显高于对照组(p<0.05).此外,与对照组相比,感染后肠易激综合征患者的白细胞介素-17(IL-17)水平升高(p<0.05)。此外,与对照组和非感染后肠易激综合征组相比,感染后肠易激综合征组表现出更高的T辅助细胞17(Th17)百分比(p<0.05).结论急性胃肠道感染可破坏肠道菌群平衡,导致生态失调。这种生态失调可以触发促炎因子的释放,包括白细胞介素-17,这有助于肠粘膜屏障的损害。因此,这为持久发展奠定了基础,轻度慢性肠道炎症,最终导致感染后肠易激综合征的发作。此外,在肠-脑轴相互作用的框架内,焦虑和抑郁可能加剧感染后肠易激综合征患者的肠道炎症.这种相互作用可以延续和延长感染后肠易激综合征患者的临床症状,进一步使病情管理复杂化。
Aims/Background The pathogenesis of irritable bowel syndrome encompasses various factors, including abnormal gastrointestinal motility, heightened visceral sensitivity, dysfunction in the brain-gut axis, psychological influences, and disturbances in the intestinal flora. These factors manifest primarily as persistent or intermittent abdominal pain, diarrhoea, alterations in bowel habits, or changes in stool characteristics. In our investigation, we delve into the repercussions of mechanical barrier damage and immune dysfunction on symptoms among patients with post-infectious irritable bowel syndrome. Methods This study recruited a total of 20 healthy controls and 49 patients diagnosed with irritable bowel syndrome. Among the irritable bowel syndrome patients, we categorised them into two groups based on the ROME IV diagnostic criteria: the post-infectious irritable bowel syndrome group (n=23) and the non-post-infectious irritable bowel syndrome group (n=26). To compare clinical features, we utilised the Gastrointestinal Symptom Rating Scale, Self-Rating Depression Scale, and Self-Rating Anxiety Scale. Furthermore, we employed various techniques including haematoxylin and eosin (HE) staining, electron microscopy, Enzyme-linked Immunosorbent Assay, and flow cytometry to assess changes in immune cells, immune factors, inflammatory biomarkers, and intestinal barrier function. Results Under haematoxylin and eosin staining, post-infectious irritable bowel syndrome patients demonstrated increased neutrophils and plasma cells compared to the control group. Additionally, electron microscopy revealed ultrastructural changes such as the widening of the epithelial cell gap in the intestinal mucosa among post-infectious irritable bowel syndrome patients. Comparatively, the Gastrointestinal Symptom Rating Scale, Self-Rating Anxiety Scale, and Self-Rating Depression Scale scores were significantly elevated in the post-infectious irritable bowel syndrome group in contrast to both the control group and the non- post-infectious irritable bowel syndrome group (p < 0.05). Moreover, post-infectious irritable bowel syndrome patients exhibited a notably higher neutrophil-to-lymphocyte ratio compared to the control group (p < 0.05). Furthermore, the levels of interleukin-17 (IL-17) were elevated in post-infectious irritable bowel syndrome patients compared to the control group (p < 0.05). Additionally, the post-infectious irritable bowel syndrome group displayed a higher percentage of T helper 17 (Th17) cells compared to both the control and non-post-infectious irritable bowel syndrome groups (p < 0.05). Conclusion Acute gastrointestinal infection can disrupt the balance of intestinal flora, leading to dysbiosis. This dysbiosis can trigger the release of pro-inflammatory factors, including interleukin-17, which contributes to the impairment of the intestinal mucosal barrier. Consequently, this sets the stage for the development of long-lasting, mild chronic intestinal inflammation, ultimately culminating in the onset of post-infectious irritable bowel syndrome. Furthermore, within the framework of the gut-brain axis interaction, anxiety and depression may exacerbate intestinal inflammation in post-infectious irritable bowel syndrome patients. This interaction can perpetuate and prolong clinical symptoms in individuals with post-infectious irritable bowel syndrome, further complicating the management of the condition.