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Updated: Sep 2, 2025
Microbiota Analysis Using Two-step PCR and Next-generation 16S rRNA Gene Sequencing
Published on: October 15, 2019
Altered Gut Microbiota in Patients With Peutz-Jeghers Syndrome
Sui Wang1,2, Gang Huang1,2, Jue-Xin Wang1,2
1Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan, China.
Insights
Gut microbiota dysbiosis is confirmed in Peutz-Jeghers syndrome (PJS) patients. This study reveals distinct bacterial and fungal profiles in PJS, offering insights into the condition's pathogenesis.
Area of Science:
- Microbiology
- Genetics
- Gastroenterology
Background:
- Peutz-Jeghers syndrome (PJS) is a rare genetic disorder linked to polyps and cancer susceptibility.
- The role of gut microbiota dysbiosis in PJS pathogenesis is currently unknown.
Purpose of the Study:
- To assess gut bacteria and fungi composition in PJS patients.
- To investigate the link between gut dysbiosis and PJS.
Main Methods:
- Fecal microbiota analyzed in 23 PJS patients, 17 asymptomatic relatives, and 24 controls.
- 16S and ITS2 sequencing used for bacterial and fungal analysis.
- Differential analysis performed from phylum to species level.
Main Results:
- PJS cases showed altered bacterial diversity and composition compared to controls and relatives.
- Specific bacterial changes include increased Proteobacteria and decreased Firmicutes.
- Fungal flora was relatively stable, but Candida was higher in PJS cases.
Conclusions:
- Gut microbiota dysbiosis is confirmed in PJS patients.
- This is the first study detailing the bacterial and fungal microbiota in PJS.
- Findings provide a basis for further research on PJS intestinal microecology.
Background:
Peutz-Jeghers syndrome (PJS) is a rare genetic disorder characterized by the development of pigmented spots and gastrointestinal polyps and increased susceptibility to cancers. It remains unknown whether gut microbiota dysbiosis is linked to PJS.
Aim:
This study aimed to assess the structure and composition of the gut microbiota, including both bacteria and fungi, in patients with PJS and investigate the relationship between gut microbiota dysbiosis and PJS pathogenesis.
Methods:
The bacterial and fungal composition of the fecal microbiota was analyzed in 23 patients with PJS (cases), 17 first-degree asymptomatic relatives (ARs), and 24 healthy controls (HCs) using 16S (MiSeq) and ITS2 (pyrosequencing) sequencing for bacteria and fungi, respectively. Differential analyses of the intestinal flora were performed from the phylum to species level.
Results:
Alpha-diversity distributions of bacteria and fungi indicated that the abundance of both taxa differed between PJS cases and controls. However, while the diversity and composition of fecal bacteria in PJS cases were significantly different from those in ARs and HCs, fungal flora was more stable. High-throughput sequencing confirmed the special characteristics and biodiversity of the fecal bacterial and fungal microflora in patients with PJS. They had lower bacterial biodiversity than controls, with a higher frequency of the Proteobacteria phylum, Enterobacteriaceae family, and Escherichia-Shigella genus, and a lower frequency of the Firmicutes phylum and the Lachnospiraceae and Ruminococcaceae families. Of fungi, Candida was significantly higher in PJS cases than in controls.
Conclusion:
The findings reported here confirm gut microbiota dysbiosis in patients with PJS. This is the first report on the bacterial and fungal microbiota profile of subjects with PJS, which may be meaningful to provide a structural basis for further research on intestinal microecology in PJS.
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