咽峡炎链球菌在幽门螺杆菌感染人群中的丰度探究

The abundance of Streptococcus anginosus in individuals infected with Helicobacter pylori

摘要:

目的 探讨幽门螺杆菌（Helicobactor pylori，HP）感染对胃黏膜和粪便中咽峡炎链球菌相对丰度的影响，并分析胃黏膜与粪便中咽峡炎链球菌丰度的相关性。方法 纳入2023年7月至2025年1月于上海交通大学医学院附属仁济医院就诊的190例HP阳性患者（HPP组）和180例HP阴性患者（CON组）。收集受试者的胃黏膜活检组织与粪便标本，采用qPCR技术检测其中咽峡炎链球菌的相对丰度。比较两组间胃黏膜与粪便中咽峡炎链球菌丰度的差异；进一步根据胃镜病理结果（浅表性胃炎、萎缩性胃炎、肠上皮化生）进行亚组分析，比较不同病理类型间及相同病理类型下两组咽峡炎链球菌丰度；最后对配对样本进行线性回归分析，探讨胃黏膜与粪便中咽峡炎链球菌丰度的关联性。结果 HPP组胃黏膜活检组织中咽峡炎链球菌的相对丰度显著低于CON组［-11.29（-12.56，-10.17）比-8.74（-10.00，-7.69），U=3 024，P<0.001］，粪便中咽峡炎链球菌的相对丰度在两组间差异无统计学意义［-14.98（-16.45，-13.80）比-14.43（-16.23，-12.95），U=5 423，P=0.225］。在不同胃黏膜病理类型下，HPP组与CON组组内胃黏膜中的咽峡炎链球菌丰度差异均无统计学意义（P>0.05）；在相同病理类型下，HPP组胃黏膜中的咽峡炎链球菌丰度均显著低于CON组［浅表性胃炎：-11.39（-12.62，-10.52）比-8.78（-10.02，-7.77），U=739，P<0.001；萎缩性胃炎：-11.19（-12.70，-9.72）比-8.78（-9.50，-8.13）， U=263，P<0.001；肠上皮化生：-10.96（-11.55，-10.25）比-8.23（-10.20，-7.09）， U=111，P<0.001］。对粪便标本的分析表明，在HPP组或CON组内，不同病理类型间的咽峡炎链球菌丰度差异无统计学意义（P>0.05）；在相同病理类型下，HPP组与CON组的咽峡炎链球菌丰度无显著差异（P>0.05）。线性回归分析显示，在HPP组（r²=0.139，P=0.017）和CON组（r²=0.211，P<0.001）中，胃黏膜与粪便中的咽峡炎链球菌丰度均存在线性关系。结论 HP感染对胃黏膜中的咽峡炎链球菌相对丰度有抑制，而粪便中咽峡炎链球菌的丰度未受到明显干扰，病理进展本身对咽峡炎链球菌丰度的影响有限。咽峡炎链球菌在配对的胃黏膜组织和粪便中的丰度变化具有一定的线性关系，粪便当中的咽峡炎链球菌丰度可以在一定程度上反映胃内咽峡炎链球菌的丰度。

Abstract:

Objective To investigate the effect of Helicobacter pylori (HP) infection on the relative abundance of Streptococcus anginosus (Sa) in gastric mucosa and feces, and to analyze their correlation. Methods A total of 190 HP-positive patients (HPP group) and 180 HP-negative patients (CON group) who visited the Renji Hopital, Shanghai Jiao Tong University School of Medicine from July 2023 to January 2025 were enrolled. Gastric mucosal biopsy tissues and fecal specimens were collected from subjects, and qPCR was used to detect the relative abundance of Sa. The differences in Sa abundance between the two groups in gastric mucosa and feces were compared. Further analyses were performed according to endoscopic pathological findings (superficial gastritis, atrophic gastritis, intestinal metaplasia) to compare Sa abundance between different pathological types and between the two groups under the same pathological type. Finally, linear regression analysis was performed on paired samples to explore the association between Sa abundance in gastric mucosa and feces. Results The relative abundance of Sa in gastric mucosal biopsy tissues of the HPP group was significantly lower than that of the CON group [-11.29 (-12.56,-10.17) VS -8.74 (-10.00, -7.69), U=3 024, P<0.001], while the relative abundance of Sa in feces showed no significant difference between the two groups [-14.98 (-16.45, -13.80) VS -14.43 (-16.23, -12.95), U=5 423, P=0.225]. Among different gastric mucosal pathological types, there was no significant difference in Sa abundance within the HPP group or within the CON group (P>0.05). However, under the same pathological type, the abundance of Sa in the gastric mucosa of the HPP group was significantly lower than that of the CON group [superficial gastritis: -11.39 (-12.62, -10.52) VS -8.78 (-10.02, -7.77), U=739, P<0.001; atrophic gastritis: -11.19 (-12.70, -9.72) VS -8.78 (-9.50, -8.13), U=263, P<0.001; intestinal metaplasia: -10.96 (-11.55, -10.25) VS -8.23 (-10.20, -7.09), U=111, P<0.001). Analysis of fecal specimens showed no significant difference in Sa abundance within different pathological types in either the HPP group or the CON group (P>0.05). Furthermore, no significant difference was found between the HPP and CON groups under the same pathological type (P>0.05). Linear regression analysis showed a linear relationship between Sa abundance in gastric mucosa and feces in both the HPP group (r²=0.139, P=0.017) and the CON group (r²=0.211, P<0.001). Conclusion HP infection has an inhibitory effect on the relative abundance of Sa in gastric mucosa, while the abundance of Sa in feces is not significantly affected. The impact of pathological progression itself on Sa abundance is limited. There is a certain linear relationship between the abundance changes of Sa in paired gastric mucosal tissue and feces, and the abundance of Sa in feces can to some extent reflect the abundance of Sa in the stomach.