Intestinal Inflammation Promotes MDL-1

Animals Antibodies, Monoclonal / metabolism Bone Resorption / genetics Cell Differentiation / physiology Cytokines / metabolism Inflammation / genetics Inflammatory Bowel Diseases / genetics Intestines / metabolism Lectins / metabolism Lectins, C-Type / genetics Mice Osteoclasts / metabolism Osteogenesis / genetics Receptors, Cell Surface / genetics
Inflammatory Bowel Disease MDL-1 Osteoclast

Journal

Cellular and molecular gastroenterology and hepatology
ISSN: 2352-345X
Titre abrégé: Cell Mol Gastroenterol Hepatol
Pays: United States
ID NLM: 101648302

Informations de publication

Date de publication:
2022
Historique:
received: 26 02 2022
revised: 01 07 2022
accepted: 05 07 2022
pubmed: 15 7 2022
medline: 28 9 2022
entrez: 14 7 2022
Statut: ppublish

Résumé

Inflammatory bowel disease (IBD) is characterized by severe gastrointestinal inflammation, but many patients experience extra-intestinal disease. Bone loss is one common extra-intestinal manifestation of IBD that occurs through dysregulated interactions between osteoclasts and osteoblasts. Systemic inflammation has been postulated to contribute to bone loss, but the specific pathologic mechanisms have not yet been fully elucidated. We hypothesized that intestinal inflammation leads to bone loss through increased abundance and altered function of osteoclast progenitors. We used chemical, T cell driven, and infectious models of intestinal inflammation to determine the impact of intestinal inflammation on bone volume, the skeletal cytokine environment, and the cellular changes to pre-osteoclast populations within bone marrow. Additionally, we evaluated the potential for monoclonal antibody treatment against an inflammation-induced osteoclast co-receptor, myeloid DNAX activation protein 12-associating lectin-1 (MDL-1) to reduce bone loss during colitis. We observed significant bone loss across all models of intestinal inflammation. Bone loss was associated with an increase in pro-osteoclastogenic cytokines within the bone and an expansion of a specific Cd11b Collectively, these data implicate the pathologic expansion and altered function of OCPs expressing MDL-1 in bone loss during IBD.

Sections du résumé

BACKGROUND & AIMS
Inflammatory bowel disease (IBD) is characterized by severe gastrointestinal inflammation, but many patients experience extra-intestinal disease. Bone loss is one common extra-intestinal manifestation of IBD that occurs through dysregulated interactions between osteoclasts and osteoblasts. Systemic inflammation has been postulated to contribute to bone loss, but the specific pathologic mechanisms have not yet been fully elucidated. We hypothesized that intestinal inflammation leads to bone loss through increased abundance and altered function of osteoclast progenitors.
METHODS
We used chemical, T cell driven, and infectious models of intestinal inflammation to determine the impact of intestinal inflammation on bone volume, the skeletal cytokine environment, and the cellular changes to pre-osteoclast populations within bone marrow. Additionally, we evaluated the potential for monoclonal antibody treatment against an inflammation-induced osteoclast co-receptor, myeloid DNAX activation protein 12-associating lectin-1 (MDL-1) to reduce bone loss during colitis.
RESULTS
We observed significant bone loss across all models of intestinal inflammation. Bone loss was associated with an increase in pro-osteoclastogenic cytokines within the bone and an expansion of a specific Cd11b
CONCLUSIONS
Collectively, these data implicate the pathologic expansion and altered function of OCPs expressing MDL-1 in bone loss during IBD.

Identifiants

DOI: 10.1016/j.jcmgh.2022.07.002 PMID: 35835390 PMC: PMC9420375
pubmed: 35835390
pii: S2352-345X(22)00160-6
doi: 10.1016/j.jcmgh.2022.07.002
pmc: PMC9420375
pii:
doi:

Substances chimiques

Antibodies, Monoclonal 0
Clec5a protein, mouse 0
Cytokines 0
Lectins 0
Lectins, C-Type 0
Receptors, Cell Surface 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

731-750

Subventions

Organisme : NIAID NIH HHS
ID : F30 AI138424
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK131104
Pays : United States
Organisme : NIDDK NIH HHS
ID : F30 DK120114
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI138932
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK105550
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007347
Pays : United States
Organisme : NIDDK NIH HHS
ID : R03 DK123489
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI168302
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK128200
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI095202
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA068485
Pays : United States
Organisme : CSRD VA
ID : I01 CX002171
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Christopher T Peek (CT)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.

Caleb A Ford (CA)

Department of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee.

Kara R Eichelberger (KR)

Department of Pediatrics, Division of Pediatric Infectious Diseases, Vanderbilt University Medical Center, Nashville, Tennessee.

Justin Jacobse (J)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Teresa P Torres (TP)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.

Damian Maseda (D)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Dermatology, University of Pennsylvania, Philadelphia, Pennsylvania.

Yvonne L Latour (YL)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.

M Blanca Piazuelo (MB)

Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Vanderbilt University Medical Center, Nashville, Tennessee.

Joshua R Johnson (JR)

Vanderbilt Center for Bone Biology, Vanderbilt University Medical Center, Nashville, Tennessee.

Mariana X Byndloss (MX)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee.

Keith T Wilson (KT)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Vanderbilt University Medical Center, Nashville, Tennessee; Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee.

Jeffrey C Rathmell (JC)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Center for Immunobiology, Vanderbilt University Medical Center, Nashville, Tennessee.

Jeremy A Goettel (JA)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Vanderbilt University Medical Center, Nashville, Tennessee.

James E Cassat (JE)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee; Department of Pediatrics, Division of Pediatric Infectious Diseases, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Center for Immunobiology, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Center for Bone Biology, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: jim.cassat@vumc.org.

Articles similaires

Evaluating the efficacy of telesurgery with dual console SSI Mantra Surgical Robotic System: experiment on animal model and clinical trials.

Sudhir Prem Srivastava, Vishwajyoti Pascual Srivastava, Avinesh Singh et al.
1.00
Robotic Surgical Procedures Animals Humans Telemedicine Models, Animal

Odour generalisation and detection dog training.

Lyn Caldicott, Thomas W Pike, Helen E Zulch et al.
1.00
Animals Odorants Dogs Generalization, Psychological Smell

Within-subject variation of C-reactive protein and high-sensitivity C-reactive protein: A systematic review and meta-analysis.

Alex Gough, Alice Sitch, Erica Ferris et al.
1.00
C-Reactive Protein Humans Biomarkers Inflammation

Prognostic value of the systemic immune-inflammation index in lung cancer patients receiving immune checkpoint inhibitors: A meta-analysis.

Yanhui Yang, Ji Li, Yi Wang et al.
1.00
Humans Immune Checkpoint Inhibitors Lung Neoplasms Prognosis Inflammation

Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Globulines › Sérum-globulines › Immunoglobulines › Anticorps › Anticorps monoclonaux › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Phénomènes physiologiques de l'appareil locomoteur et du système nerveux › Phénomènes physiologiques du système locomoteur › Résorption osseuse › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Différenciation cellulaire › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Cytokines › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Inflammation › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Maladies de l'appareil digestif › Maladies gastro-intestinales › Maladies intestinales › Maladies inflammatoires intestinales › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Système digestif › Tube digestif › Intestins › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Lectines › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Lectines › Lectines de type C › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Cellules › Cellules myéloïdes › Ostéoclastes › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Phénomènes physiologiques de l'appareil locomoteur et du système nerveux › Phénomènes physiologiques du système locomoteur › Développement locomoteur › Biominéralisation › Développement osseux › Ostéogenèse › Intestinal Inflammation Promotes MDL-1
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Intestinal Inflammation Promotes MDL-1