Altered intestinal microbiota enhances adenoid hypertrophy by disrupting the immune balance

Front Immunol. 2023 Nov 28:14:1277351. doi: 10.3389/fimmu.2023.1277351. eCollection 2023.

Abstract

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.

Keywords: adenoid hypertrophy; children; fecal microbiome transplantation; gut microbiota; immune response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoids*
  • Animals
  • Bacteroides / genetics
  • Child
  • Gastrointestinal Microbiome* / physiology
  • Humans
  • Hypertrophy
  • Mice
  • Microbiota*
  • RNA, Ribosomal, 16S / genetics

Substances

  • RNA, Ribosomal, 16S

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the Shanghai Municipal Key Clinical Specialty (shslczdzk06902) and Natural Science Foundation of Shanghai (21ZR1452900).