The gut microbiota-SCFA-inflammation axis in patients with AECOPD

Hengjing Zhu1, Chen Wu2, Haiyan Wu3

  • 1Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, China.

Plos One
|January 9, 2025
PubMed
Abstract

Insights

Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is linked to gut microbiota changes, reduced short-chain fatty acids (SCFAs), and inflammation. This study explores the gut microbiota-SCFA-inflammation axis in AECOPD patients.

Area of Science:

  • Microbiome research
  • Gastroenterology
  • Pulmonary medicine

Background:

  • The gut microbiota plays a crucial role in maintaining host health.
  • Alterations in gut microbiota composition have been associated with various inflammatory conditions.
  • Understanding the gut microbiota's role in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is important for potential therapeutic strategies.

Purpose of the Study:

  • To investigate changes in gut microbiota and short-chain fatty acids (SCFAs) in patients with AECOPD.
  • To examine the relationship between gut microbiota alterations, SCFA levels, and inflammation in AECOPD.
  • To test the hypothesis that gut dysbiosis exacerbates inflammation in AECOPD.

Main Methods:

  • Gut microbiota composition was analyzed using 16S rDNA sequencing.
  • Serum inflammatory markers were measured via ELISA.
  • Short-chain fatty acid (SCFA) concentrations in the gut lumen were determined by gas chromatography-mass spectrometry.

Main Results:

  • AECOPD patients exhibited decreased gut microbiota richness and diversity compared to healthy controls.
  • Significant differences in gut microbiota composition (β-diversity) were observed between AECOPD patients and controls.
  • SCFA levels were reduced in AECOPD patients, and only IL-6 showed a reduction among measured inflammatory markers.

Conclusions:

  • AECOPD is associated with an imbalanced gut microbiota-SCFA-inflammation axis.
  • Reduced gut microbiota diversity and abundance in AECOPD patients lead to decreased SCFAs.
  • This dysregulation contributes to an inflammatory imbalance in AECOPD.

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