Feng Yanhai, Huang Yalan, Wang Yu, Wang Pei, Wang Fengjun
1State Key Laboratory of Trauma, Burns, and Combined Injury, Institute of Burn Research, Southwest Hospital, Third Military Medical University (Army Medical University), 30 Gaotanyan Street, Chongqing, 400038 China.
2Department of Military Nursing, School of Nursing, Third Military Medical University (Army Medical University), Chongqing, China.
Burns Trauma. 2019 Jul 4;7:20. doi: 10.1186/s41038-019-0156-1. eCollection 2019.
The intestinal barrier integrity is crucial for maintaining intestinal homeostasis, and the mechanisms of intestinal barrier disruption induced by burn injury remain obscure. This study was aimed to investigate the changes of intestinal microbiota and barrier function in burned mice to further comprehend the mechanisms of burn-induced intestinal barrier dysfunction.
Samples were from mice inflicted with 30% total body surface area (TBSA) full-thickness burns. The intestinal permeability, tight junction proteins expressions, zonula occludens-1 (ZO-1) localization, inflammatory cytokines expressions, and short-chain fatty acids (SCFAs) contents were determined. The microbial community was assessed via 16S rDNA Illumina sequencing.
The intestinal permeability was increased after severe burn injury, peaking at 6 h post-burn, with approximately 20-folds of the control ( < 0.001). The expression of tight junction proteins (ZO-1, occludin, claudin-1, and claudin-2) was significantly altered ( < 0.05). The ZO-1 morphology was dramatically changed following burn injury. The fecal SCFAs' contents (acetate, propionate, butyrate, isobutyrate, and isovalerate) were noticeably declined after burn injury ( < 0.05). The expressions of pro-inflammatory cytokines (interleukin (IL)-1β and IL-6) in ileal mucosa were increased, whereas the expressions of anti-inflammatory cytokines (IL-4 and IL-13) were decreased following burn injury ( < 0.05). In addition, burned mice showed an alteration of intestinal microbial community, such as decreased diversity, reduced abundance, and increased abundance.
The severe burn-induced intestinal barrier dysfunction is along with the alterations of microbial community.
肠道屏障完整性对于维持肠道稳态至关重要,而烧伤所致肠道屏障破坏的机制仍不清楚。本研究旨在探讨烧伤小鼠肠道微生物群和屏障功能的变化,以进一步理解烧伤诱导的肠道屏障功能障碍的机制。
样本取自全身表面积(TBSA)30%的全层烧伤小鼠。测定肠道通透性、紧密连接蛋白表达、闭锁小带蛋白1(ZO-1)定位、炎性细胞因子表达和短链脂肪酸(SCFA)含量。通过16S rDNA Illumina测序评估微生物群落。
严重烧伤后肠道通透性增加,在烧伤后6小时达到峰值,约为对照组的20倍(<0.001)。紧密连接蛋白(ZO-1、闭合蛋白、claudin-1和claudin-2)的表达显著改变(<0.05)。烧伤后ZO-1形态发生显著变化。烧伤后粪便SCFA含量(乙酸盐、丙酸盐、丁酸盐、异丁酸盐和异戊酸盐)明显下降(<0.05)。烧伤后回肠黏膜促炎细胞因子(白细胞介素(IL)-1β和IL-6)的表达增加,而抗炎细胞因子(IL-4和IL-13)的表达降低(<0.05)。此外,烧伤小鼠肠道微生物群落发生改变,如多样性降低、丰度减少和丰度增加。
严重烧伤诱导的肠道屏障功能障碍与微生物群落的改变有关。