Faecal microbial transfer and complex carbohydrates mediate protection against COPDOriginal paper
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreWhat was studied?
Researchers examined whether the gut microbiome contributes to chronic obstructive pulmonary disease (COPD) pathogenesis, using a mouse model of cigarette smoke-induced COPD and a small human pilot trial of inulin supplementation.
How was it studied?
Mice with cigarette smoke-induced COPD received faecal microbial transfer (FMT), with faecal microbiota profiled by metagenomics, proteomics and metabolomics; findings were linked to airway and systemic inflammation, lung and gut histopathology, and lung function. A high resistant starch diet was tested in mice, and 16 COPD patients received a randomised, double-blind, placebo-controlled pilot trial of inulin.
What did they find?
FMT alleviated inflammation, alveolar destruction, impaired lung function, gut pathology, and systemic immune changes, with effects additive to smoking cessation. Disease features correlated with relative abundance of Muribaculaceae, Desulfovibrionaceae and Lachnospiraceae, and proteomics/metabolomics showed downregulated glucose and starch metabolism in smoke-associated microbiota; complex carbohydrate supplementation improved outcomes in both mice and patients.
Why it matters
The findings indicate the gut microbiome actively drives COPD pathogenesis via the gut-lung axis and suggest microbiome-targeted interventions, such as complex carbohydrate supplementation, as a potential therapeutic strategy.