Altered gut microbiota in the early stage of acute pancreatitis were related to the occurrence of acute respiratory distress syndrome

Front Cell Infect Microbiol. 2023 Mar 6:13:1127369. doi: 10.3389/fcimb.2023.1127369. eCollection 2023.


Background: Acute respiratory distress syndrome (ARDS) is the most common cause of organ failure in acute pancreatitis (AP) patients, which associated with high mortality. Specific changes in the gut microbiota have been shown to influence progression of acute pancreatitis. We aimed to determine whether early alterations in the gut microbiota is related to and could predict ARDS occurrence in AP patients.

Methods: In this study, we performed 16S rRNA sequencing analysis in 65 AP patients and 20 healthy volunteers. The AP patients were further divided into two groups: 26 AP-ARDS patients and 39 AP-nonARDS patients based on ARDS occurrence during hospitalization.

Results: Our results showed that the AP-ARDS patients exhibited specific changes in gut microbiota composition and function as compared to subjects of AP-nonARDS group. Higher abundances of Proteobacteria phylum, Enterobacteriaceae family, Escherichia-Shigella genus, and Klebsiella pneumoniae, but lower abundances of Bifidobacterium genus were found in AP-ARDS group compared with AP-nonARDS groups. Random forest modelling analysis revealed that the Escherichia-shigella genus was effective to distinguish AP-ARDS from AP-nonARDS, which could predict ARDS occurrence in AP patients.

Conclusions: Our study revealed that alterations of gut microbiota in AP patients on admission were associated with ARDS occurrence after hospitalization, indicating a potential predictive and pathogenic role of gut microbiota in the development of ARDS in AP patients.

Keywords: acute pancreatitis; acute respiratory distress syndrome; biomarker; disease prediction; gut microbiota.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Gastrointestinal Microbiome*
  • Humans
  • Pancreatitis* / complications
  • RNA, Ribosomal, 16S / genetics
  • Respiratory Distress Syndrome* / etiology


  • RNA, Ribosomal, 16S

Grants and funding

This study was supported by grants from Chinese Natural Science Foundation, grant number 82270405 and 32170788, National Key Clinical Specialty Construction Project, grant number ZK108000, National High Level Hospital Clinical Research Funding, grant number 2022-PUMCH-A-026, 2022-PUMCH-B-016, 2022-PUMCH-B-023, and Beijing Nova Program.