Li Wenjie, Qing Yong, Yu Qiuyue, Zhang Hulian, Rang Zhen, Li Shuangli, Cui Fan
School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Institute of Dermatology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China.
Can J Infect Dis Med Microbiol. 2024 Dec 9;2024:6995192. doi: 10.1155/cjid/6995192. eCollection 2024.
Damage to the intestinal mucosal barrier and dysbiosis of the gut microbiota are critical factors in HIV progression, reciprocally influencing each other. Besides bacteria, the fungal microbiota, a significant component of the gut, plays a pivotal role in this dysregulation. This study aims to investigate changes in the gut mucosal barrier and mycobiota during the initial stages of HIV infection, focusing on the involvement of intestinal fungi and their secretions in mucosal damage. Peripheral blood, intestinal mucosa, and fecal samples were collected from 13 asymptomatic HIV-infected individuals at the non-AIDS stage and 13 healthy controls. Assessments included colonoscopy, immune function analysis, and measurement of mucosal damage markers (LPS, I-FABP, and D-LA) and inflammatory cytokines (IL-6 and IL-18). Additionally, Claudin-1 levels in mucosal samples and fungal profiles in fecal samples were evaluated. The study found that colonic abnormalities were significantly more prevalent in the HIV group compared to healthy controls ( < 0.001) and Claudin-1 levels were notably lower in the HIV group ( < 0.001). (=0.0084), its secretion SAP1 (=0.023), and the levels of IL-18 (=0.0016) and IL-6 ( < 0.001) were all significantly higher in the HIV group. CD4+ T-cell counts were positively correlated with Claudin-1 expression (=0.034, = 0.417). showed negative correlations with several virulence factors, while other fungi exhibited varied correlations. Additionally, Claudin-1 levels were significantly negatively correlated with (=0.013, = -0.668), SAP1 (=0.027, = -0.609), IL-18 ( < 0.001, = -0.922), and IL-6 ( < 0.001, = -0.920). Overall, these findings suggest that asymptomatic HIV-infected individuals have already exhibited intestinal mucosal damage in the early stage and highlight the critical role of and its secretions in early-stage intestinal mucosal barrier damage.
肠道黏膜屏障受损和肠道微生物群失调是HIV病情进展的关键因素，二者相互影响。除细菌外，肠道重要组成部分的真菌微生物群在这种失调中起关键作用。本研究旨在调查HIV感染初期肠道黏膜屏障和真菌群的变化，重点关注肠道真菌及其分泌物在黏膜损伤中的作用。收集了13名处于非艾滋病阶段的无症状HIV感染者和13名健康对照者的外周血、肠道黏膜及粪便样本。评估包括结肠镜检查、免疫功能分析以及黏膜损伤标志物（脂多糖、肠脂肪酸结合蛋白和D-乳酸）和炎性细胞因子（白细胞介素-6和白细胞介素-18）的检测。此外，还评估了黏膜样本中Claudin-1水平和粪便样本中的真菌谱。研究发现，与健康对照相比，HIV组结肠异常更为普遍（<0.001），HIV组Claudin-1水平显著更低（<0.001）。HIV组中，某真菌（=0.0084）、其分泌的SAP1（=0.023）以及白细胞介素-18（=0.0016）和白细胞介素-6（<0.001）的水平均显著更高。CD4 + T细胞计数与Claudin-1表达呈正相关（=0.034，=0.417）。某真菌与几种毒力因子呈负相关，而其他真菌表现出不同的相关性。此外，Claudin-1水平与某真菌（=0.013，=-0.668）、SAP1（=0.027，=-0.609）、白细胞介素-18（<0.001，=-0.922）和白细胞介素-6（<0.001，=-0.920）均呈显著负相关。总体而言，这些发现表明无症状HIV感染者在早期已出现肠道黏膜损伤，并突出了某真菌及其分泌物在早期肠道黏膜屏障损伤中的关键作用。
