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Published on: December 16, 2021
Altered intestinal microbiota enhances adenoid hypertrophy by disrupting the immune balance
Wenxin Liu1,2, Huier Jiang1,2, Xiling Liu3
1Department of Clinical Laboratory, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Insights
Altered gut microbiota is linked to adenoid hypertrophy (AH) in children. Fecal microbiome transplantation in mice demonstrated that gut bacteria influence immune responses relevant to AH.
Area of Science:
- Pediatric respiratory health
- Microbiome research
- Immunology
Background:
- Adenoid hypertrophy (AH) is a prevalent pediatric respiratory condition.
- Gut microbiota alterations are suspected contributors to AH, but the precise relationship is unclear.
Purpose of the Study:
- To investigate the gut microbiome composition in children with AH.
- To explore the functional impact of AH-associated gut microbiota on immune responses.
Main Methods:
- 16S rRNA gene sequencing of fecal samples from 119 children with AH and 100 healthy controls.
- Fecal microbiome transplantation (FMT) in mice to assess immune effects.
Main Results:
- Significant differences in gut microbial composition between AH patients and controls, with specific genera like Akkermansia and Faecalibacterium showing altered abundance.
- A panel of 8 OTUs accurately distinguished AH from healthy controls (AUC > 0.97).
- FMT from AH patients altered Treg and Th2 cell populations in mice, suggesting a role in immune dysregulation.
Conclusions:
- The gut microbiota plays a significant role in the pathogenesis of adenoid hypertrophy.
- Specific microbial signatures may serve as diagnostic markers for AH.
Introduction:
Adenoid hypertrophy (AH) is a common upper respiratory disorder in children. Disturbances of gut microbiota have been implicated in AH. However, the interplay of alteration of gut microbiome and enlarged adenoids remains elusive.
Methods:
119 AH children and 100 healthy controls were recruited, and microbiome profiling of fecal samples in participants was performed using 16S rRNA gene sequencing. Fecal microbiome transplantation (FMT) was conducted to verify the effects of gut microbiota on immune response in mice.
Results:
In AH individuals, only a slight decrease of diversity in bacterial community was found, while significant changes of microbial composition were observed between these two groups. Compared with HCs, decreased abundances of Akkermansia, Oscillospiraceae and Eubacterium coprostanoligenes genera and increased abundances of Bacteroides, Faecalibacterium, Ruminococcus gnavus genera were revealed in AH patients. The abundance of Bacteroides remained stable with age in AH children. Notably, a microbial marker panel of 8 OTUs were identified, which discriminated AH from HC individuals with an area under the curve (AUC) of 0.9851 in the discovery set, and verified in the geographically different validation set, achieving an AUC of 0.9782. Furthermore, transfer of mice with fecal microbiota from AH patients dramatically reduced the proportion of Treg subsets within peripheral blood and nasal-associated lymphoid tissue (NALT) and promoted the expansion of Th2 cells in NALT.
Conclusion:
These findings highlight the effect of the altered gut microbiota in the AH pathogenesis.
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