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Gut microbiota, metabolome and immune signatures in patients with uncomplicated diverticular disease
  1. Giovanni Barbara1,
  2. Eleonora Scaioli1,
  3. Maria Raffaella Barbaro1,
  4. Elena Biagi2,
  5. Luca Laghi3,
  6. Cesare Cremon1,
  7. Giovanni Marasco1,
  8. Antonio Colecchia1,
  9. Gianfranco Picone3,
  10. Nunzio Salfi4,
  11. Francesco Capozzi3,
  12. Patrizia Brigidi2,
  13. Davide Festi1
  1. 1Department of Medical and Surgical Sciences, S.Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy
  2. 2Department of Pharmacy and Biotechnology, S.Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy
  3. 3Department of Agri-Food Sciences and Technologies, S.Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy
  4. 4Pathology Unit, S.Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy
  1. Correspondence to Dr Giovanni Barbara, Department of Medical and Surgical Sciences, St. Orsola-Malpighi Hospital—Via Massarenti, 9—Building #5, Bologna I-40138, Italy; giovanni.barbara{at}unibo.it

Abstract

Objective The engagement of the gut microbiota in the development of symptoms and complications of diverticular disease has been frequently hypothesised. Our aim was to explore colonic immunocytes, gut microbiota and the metabolome in patients with diverticular disease in a descriptive, cross-sectional, pilot study.

Design Following colonoscopy with biopsy and questionnaire phenotyping, patients were classified into diverticulosis or symptomatic uncomplicated diverticular disease; asymptomatic subjects served as controls. Mucosal immunocytes, in the diverticular region and in unaffected sites, were quantified with immunohistochemistry. Mucosa and faecal microbiota were analysed by the phylogenetic platform high taxonomic fingerprint (HTF)-Microbi.Array, while the metabolome was assessed by 1H nuclear magnetic resonance.

Results Compared with controls, patients with diverticula, regardless of symptoms, had a >70% increase in colonic macrophages. Their faecal microbiota showed depletion of Clostridium cluster IV. Clostridium cluster IX, Fusobacterium and Lactobacillaceae were reduced in symptomatic versus asymptomatic patients. A negative correlation was found between macrophages and mucosal Clostridium cluster IV and Akkermansia. Urinary and faecal metabolome changes in diverticular disease involved the hippurate and kynurenine pathways. Six urinary molecules allowed to discriminate diverticular disease and control groups with >95% accuracy.

Conclusions Patients with colonic diverticular disease show depletion of microbiota members with anti-inflammatory activity associated with mucosal macrophage infiltration. Metabolome profiles were linked to inflammatory pathways and gut neuromotor dysfunction and showed the ability to discriminate diverticular subgroups and controls. These data pave the way for further large-scale studies specifically aimed at identifying microbiota signatures with a potential diagnostic value in patients with diverticular disease.

  • DIVERTICULAR DISEASE
  • MACROPHAGES
  • COLONIC MICROFLORA
  • INTESTINAL MICROBIOLOGY
  • COLONIC MUCOSAL METABOLISM

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