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@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},
}