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Study on the additive protective effect of PGLYRP3 and Bifidobacterium adolescentis Reuter 1963 on severity of DSS-induced colitis in Pglyrp3 knockout (Pglyrp3 -/-) and wild-type (WT) mice.

  • Ghadimi, Darab1
  • de Vrese, Michael2
  • Ebsen, Michael3
  • Röcken, Christoph4
  • Olaf Frahm, Sven5
  • Zahlten, Janine6
  • Fölster-Holst, Regina7
  • Heller, Knut J2
  • Bockelmann, Wilhelm2
  • 1 Department of Microbiology and Biotechnology, Max Rubner-Institut, Hermann-Weigmann-Str 1, D-24103 Kiel, Germany. Electronic address: [email protected] , (Germany)
  • 2 Department of Microbiology and Biotechnology, Max Rubner-Institut, Hermann-Weigmann-Str 1, D-24103 Kiel, Germany. , (Germany)
  • 3 Städtisches MVZ Kiel GmbH, Department of Pathology, Chemnitzstr.33, 24116 Kiel, Germany. , (Germany)
  • 4 Institute of Pathology, Kiel University, University Hospital, Schleswig-Holstein, Arnold-Heller-Straße 3/14, D-24105 Kiel, Germany. , (Germany)
  • 5 Medizinisches Versorgungszentrum (MVZ), Pathology and Laboratory Medicine Dr. Rabenhorst, Prüner Gang 7, 24103 Kiel, Germany. , (Germany)
  • 6 Department of Infectious Diseases and Respiratory Medicine, Charité - Universitätsmedizin, Augustenburger Platz 1, 13353 Berlin, Germany. , (Germany)
  • 7 Clinic of Dermatology, University Hospital Schleswig-Holstein, Schittenhelmstr. 7, D-24105 Kiel, Germany. , (Germany)
Published Article
Publication Date
Nov 12, 2020
DOI: 10.1016/j.imbio.2020.152028
PMID: 33242664


Pglyrp3 is a bactericidal innate immunity protein known to sustain the habitual gut microbiome and protect against experimental colitis. Intestinal inflammation and metaflammation are commonly associated with a marked reduction of commensal bifidobacteria. Whether Pglyrp3 and bifidobacteria interact synergistically or additively to alleviate metaflammation is unknown. We investigated the extent to which Pglyrp3 and bifidobacteria regulate metaflammation and gut bacterial dysbiosis in DSS-induced mouse models of intestinal inflammation. 8-10 weeks old male mice were used. In both WT and Pglyrp3 -/- experiments, the mice were randomly divided into three groups of 16 mice per group: (1) a control group receiving sterile tap water, (2) an experimental group receiving sterile tap water supplemented with only 5% DSS, and (3) an experimental group receiving sterile tap water supplemented with 5% DSS and 1 × 109 CFU/ml of Bifidobacterium adolescentis (B.a.) for 7 days. Wild-type (WT) littermates of the respective gene (i.e. Pglyrp3) were used as controls throughout the study. Clinical signs of general health and inflammation were monitored daily. Faecal pellet samples were analysed by qRT-PCR for microbial composition. Histology of relevant organs was carried out on day 8. Metabolic parameters and liver inflammation were determined in serum samples. Intestinal inflammation in mice of group 2 were significantly increased compared to those of control group 1. There was a significant difference in mean scores for inflammation severity between DSS-treated WT and DSS-treated Pglyrp3 -/- mice. Buildup of key serum metabolic markers (cholesterol, triglyceride and glucose) was set off by colonic inflammation. qRT-PCR quantification showed that DSS significantly decreased the Clostridium coccoides and Bifidobacterium cell counts while increasing those of Bacteroides group in both WT and Pglyrp3 -/- mice. These manifestations of DSS-induced dysbiosis were significantly attenuated by feeding B.a. Both the local and systemic ill-being of the mice alleviated when they received B.a. This study shows that Pglyrp3 facilitates recognition of bifidobacterial cell wall-derived peptidoglycan, thus leading additively to a reduction of metaflammation through an increase in the number of bifidobacteria, which were able to mitigate intestinal immunopathology in the context of Pglyrp3 blockade. Copyright © 2020 Elsevier GmbH. All rights reserved.

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