Tian Zhiying, Deng Ting, Gui Xuwen, Wang Leilei, Yan Qiulong, Wang Liang
Stem Cell Clinical Research Center, National Joint Engineering Laboratory, Regenerative Medicine Center, The First Affiliated Hospital of Dalian Medical University, No. 193, Lianhe Road, Shahekou District, Dalian 116011, China.
Department of Biotechnology, College of Basic Medical Science, Dalian Medical University, Dalian 116044, China.
Microorganisms. 2023 Aug 31;11(9):2203. doi: 10.3390/microorganisms11092203.
Bacterial pneumonia is the main cause of illness and death in children under 5 years old. We isolated and cultured pathogenic bacteria from the intestines of children with pneumonia and replicated the pediatric pneumonia model using an oral gavage bacterial animal model. Interestingly, based on 16srRNA sequencing, we found that the gut and lung microbiota showed the same imbalance trend, which weakened the natural resistance of this area. Further exploration of its mechanism revealed that the disruption of the intestinal mechanical barrier led to the activation of inflammatory factors IL-6 and IL-17, which promoted the recruitment of ILC-3 and the release of IL-17 and IL-22, leading to lung inflammation. The focus of this study is on the premise that the gut and lung microbiota exhibit similar destructive changes, mediating the innate immune response to promote the occurrence of pneumonia and providing a basis for the development and treatment of new drugs for pediatric pneumonia.
细菌性肺炎是5岁以下儿童患病和死亡的主要原因。我们从肺炎患儿的肠道中分离并培养了病原菌，并使用口服灌胃细菌动物模型复制了小儿肺炎模型。有趣的是，基于16srRNA测序，我们发现肠道和肺部微生物群呈现相同的失衡趋势，这削弱了该区域的天然抵抗力。对其机制的进一步探索表明，肠道机械屏障的破坏导致炎症因子IL-6和IL-17的激活，促进了ILC-3的募集以及IL-17和IL-22的释放，从而导致肺部炎症。本研究的重点是基于肠道和肺部微生物群呈现相似的破坏性变化这一前提，介导先天性免疫反应以促进肺炎的发生，并为小儿肺炎新药的研发和治疗提供依据。
