Mechanisms of Lung and Intestinal Microbiota and Innate Immune Changes Caused by Pathogenic Enterococcus Faecalis
Zhiying Tian1, Ting Deng2, Xuwen Gui2
1Stem 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.
Insights
Pediatric pneumonia in children under 5 is linked to gut bacteria imbalance. This imbalance weakens natural defenses, leading to lung inflammation and disease progression.
Area of Science:
- Microbiology
- Immunology
- Pediatrics
Background:
- Bacterial pneumonia is a leading cause of mortality in children under five.
- Gut microbiota dysbiosis is increasingly recognized as a factor in various diseases.
Purpose of the Study:
- To investigate the link between gut microbiota imbalance and pediatric pneumonia.
- To elucidate the underlying mechanisms of pneumonia development in a pediatric model.
Main Methods:
- Isolation and culturing of pathogenic bacteria (LE) from children with pneumonia.
- Development of a pediatric pneumonia animal model using oral gavage.
- 16S rRNA sequencing to analyze gut and lung microbiota composition.
Main Results:
- Identified pathogenic bacteria LE from children with pneumonia.
- Observed similar gut and lung microbiota imbalance trends in the pneumonia model.
- Demonstrated that intestinal barrier disruption activates IL-6 and IL-17, promoting ILC-3 recruitment and IL-17/IL-22 release, causing lung inflammation.
Conclusions:
- Gut and lung microbiota share similar dysbiotic changes in pediatric pneumonia.
- Innate immune responses, driven by gut-lung axis dysbiosis, contribute to pneumonia pathogenesis.
- Findings provide a basis for novel therapeutic strategies targeting pediatric pneumonia.
Abstract:
Bacterial pneumonia is the main cause of illness and death in children under 5 years old. We isolated and cultured pathogenic bacteria LE 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.
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