% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Budden:268848,
author = {Budden, Kurtis F and Shukla, Shakti D and Bowerman, Kate L
and Vaughan, Annalicia and Gellatly, Shaan L and Wood, David
L A and Lachner, Nancy and Idrees, Sobia and Rehman, Saima
Firdous and Faiz, Alen and Patel, Vyoma K and Donovan,
Chantal and Alemao, Charlotte A and Shen, Sj and Amorim,
Nadia and Majumder, Rajib and Vanka, Kanth S and Mason, Jazz
and Haw, Tatt Jhong and Tillet, Bree and Fricker, Michael
and Keely, Simon and Hansbro, Nicole and Belz, Gabrielle T
and Horvat, Jay and Ashhurst, Thomas and van Vreden, Caryn
and McGuire, Helen and Fazekas de St Groth, Barbara and
King, Nicholas J C and Crossett, Ben and Cordwell, Stuart J
and Bonaguro, Lorenzo and Schultze, Joachim L and
Hamilton-Williams, Emma E and Mann, Elizabeth and Forster,
Samuel C and Cooper, Matthew A and Segal, Leopoldo N and
Chotirmall, Sanjay H and Collins, Peter and Bowman, Rayleen
and Fong, Kwun M and Yang, Ian A and Wark, Peter A B and
Dennis, Paul G and Hugenholtz, Philip and Hansbro, Philip M},
title = {{F}aecal microbial transfer and complex carbohydrates
mediate protection against {COPD}.},
journal = {Gut},
volume = {73},
number = {5},
issn = {0017-5749},
address = {London},
publisher = {BMJ Publishing Group},
reportid = {DZNE-2024-00352},
pages = {751 - 769},
year = {2024},
abstract = {Chronic obstructive pulmonary disease (COPD) is a major
cause of global illness and death, most commonly caused by
cigarette smoke. The mechanisms of pathogenesis remain
poorly understood, limiting the development of effective
therapies. The gastrointestinal microbiome has been
implicated in chronic lung diseases via the gut-lung axis,
but its role is unclear.Using an in vivo mouse model of
cigarette smoke (CS)-induced COPD and faecal microbial
transfer (FMT), we characterised the faecal microbiota using
metagenomics, proteomics and metabolomics. Findings were
correlated with airway and systemic inflammation, lung and
gut histopathology and lung function. Complex carbohydrates
were assessed in mice using a high resistant starch diet,
and in 16 patients with COPD using a randomised,
double-blind, placebo-controlled pilot study of inulin
supplementation.FMT alleviated hallmark features of COPD
(inflammation, alveolar destruction, impaired lung
function), gastrointestinal pathology and systemic immune
changes. Protective effects were additive to smoking
cessation, and transfer of CS-associated microbiota after
antibiotic-induced microbiome depletion was sufficient to
increase lung inflammation while suppressing colonic
immunity in the absence of CS exposure. Disease features
correlated with the relative abundance of Muribaculaceae,
Desulfovibrionaceae and Lachnospiraceae family members.
Proteomics and metabolomics identified downregulation of
glucose and starch metabolism in CS-associated microbiota,
and supplementation of mice or human patients with complex
carbohydrates improved disease outcomes.The gut microbiome
contributes to COPD pathogenesis and can be targeted
therapeutically.},
keywords = {Humans / Mice / Animals / Pulmonary Disease, Chronic
Obstructive: etiology / Lung: metabolism / Lung: pathology /
Pneumonia: etiology / Inflammation: metabolism /
Carbohydrates: pharmacology / BASIC SCIENCES (Other) /
COLONIC MICROFLORA (Other) / DIETARY FIBRE (Other) /
IMMUNOLOGY (Other) / INFLAMMATORY DISEASES (Other) /
Carbohydrates (NLM Chemicals)},
cin = {AG Schultze / Schultze - PRECISE},
ddc = {610},
cid = {I:(DE-2719)1013038 / I:(DE-2719)1013031},
pnm = {354 - Disease Prevention and Healthy Aging (POF4-354) / 352
- Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-354 / G:(DE-HGF)POF4-352},
experiment = {EXP:(DE-2719)PRECISE-20190321},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:38331563},
doi = {10.1136/gutjnl-2023-330521},
url = {https://pub.dzne.de/record/268848},
}