Evidence map›Paper›PMID 35835390›Full record

ArticleCellular and molecular gastroenterology and hepatology2022

Intestinal Inflammation Promotes MDL-1

Christopher T Peek, Caleb A Ford, Kara R Eichelberger, Justin Jacobse, Teresa P Torres, Damian Maseda, Yvonne L Latour, M Blanca Piazuelo, Joshua R Johnson, Mariana X Byndloss and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. The gut-bone-inflammation axis: intestinal barrier disruption as a central driver of osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
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  16. Bone Loss in Intestinal Inflammation Disease Yields to Osteoclastogenesis Inhibition.Cellular and molecular gastroenterology and hepatology · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Christopher T PeekDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Caleb A FordDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee.
Kara R EichelbergerDepartment of Pediatrics, Division of Pediatric Infectious Diseases, Vanderbilt University Medical Center, Nashville, Tennessee.
Justin JacobseDepartment 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 TorresDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Damian MasedaDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Dermatology, University of Pennsylvania, Philadelphia, Pennsylvania.
Yvonne L LatourDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
M Blanca PiazueloDivision 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 JohnsonVanderbilt Center for Bone Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
Mariana X ByndlossDepartment 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 WilsonDepartment 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 RathmellDepartment 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 GoettelDepartment 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 CassatDepartment 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.
Vanderbilt University Medical Center · USVanderbilt University · USUniversity of Pennsylvania · USVA Tennessee Valley Healthcare System · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Medical Scientist Training ProgramT32GM152284 · NIGMS · VANDERBILT UNIVERSITY · PI Christopher S. Williams · 2024 to 2026
$4.8M
Exploiting metabolic vulnerabilities of CD4 T cell subsets to control inflammatory diseaseR01DK105550 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Jeffrey C Rathmell · 2015 to 2026
$4.7M
Childhood Infections Research ProgramT32AI095202 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI JAMES E CASSAT · 2011 to 2026
$4.2M
Spermidine as a New Therapy for Colitis and Chemopreventive for Colitis-associated CarcinogenesisR01DK128200 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, KEITH T. · 2021 to 2024
$2.7M
Mechanisms of Salmonella-mediated disruption of colonization resistance in the inflamed gutR01AI168302 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Mariana Xavier Byndloss · 2022 to 2026
$2.4M
Obesogenic diet-induced intestinal epithelium repair responses link dysbiosis and cardiovascular diseaseR01DK131104 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Mariana Xavier Byndloss · 2022 to 2026
$2.4M
Immunological Mechanisms of Disease Training ProgramT32AI138932 · NIAID · VANDERBILT UNIVERSITY · PI MAJOR, AMY S, RATHMELL, JEFFREY C. · 2019 to 2023
$1.4M
Investigating the Role of IL-23R in Mucosal Regulatory T CellsR03DK123489 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GOETTEL, JEREMY ALLEN · 2020 to 2021
$260k
The impact of dysbiosis and the IL-12/23 signaling axis on IBD-associated bone loss.F30DK120114 · NIDDK · VANDERBILT UNIVERSITY · PI PEEK, CHRISTOPHER THOMAS · 2019 to 2022
$159k
CSRD VA I01 CX002171NCI NIH HHS P30 CA068485NIAID NIH HHS F30 AI138424NIAID NIH HHS R01 AI168302NIAID NIH HHS T32 AI095202NIAID NIH HHS T32 AI138932NIDDK NIH HHS F30 DK120114NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK105550NIDDK NIH HHS R01 DK128200NIDDK NIH HHS R01 DK131104NIDDK NIH HHS R03 DK123489NIGMS NIH HHS T32 GM007347NIGMS NIH HHS T32 GM152284
6 · The paper itself

Abstract

BACKGROUND &

aimsInflammatory 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.

methodsWe 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.

resultsWe 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

conclusionsCollectively, these data implicate the pathologic expansion and altered function of OCPs expressing MDL-1 in bone loss during IBD.

Indexed as

Bone ResorptionInflammatory Bowel DiseasesLectins, C-TypeOsteoclastsOsteogenesisReceptors, Cell SurfaceAnimalsAntibodies, MonoclonalCell DifferentiationCytokinesInflammationIntestinesLectinsMiceAntibodies, MonoclonalClec5a protein, mouseCytokinesLectinsLectins, C-TypeReceptors, Cell SurfaceInflammatory Bowel DiseaseMDL-1Osteoclast

Identifiers

PMID35835390
PMCPMC9420375
OpenAlexW4285023356

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.