Evidence map›Paper›PMID 26170381›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

β-Glucuronidase, a Regulator of Lyme Arthritis Severity, Modulates Lysosomal Trafficking and MMP-9 Secretion in Response to Inflammatory Stimuli.

Kenneth K C Bramwell, Kelton Mock, Ying Ma, John H Weis, Cory Teuscher, Janis J Weis

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Unlocking the Neuroprotective Potential ofAntioxidants (Basel, Switzerland) · 2026
    Review
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  11. Article
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  13. Article
  14. Frontiers in immunology · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Kenneth K C BramwellDivision of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT 84112;
Kelton MockUniversity of Puget Sound, Tacoma, WA 98416; and.
Ying MaDivision of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT 84112;
John H WeisDivision of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT 84112;
Cory TeuscherDepartment of Medicine, University of Vermont, Burlington, VT 05405.
Janis J WeisDivision of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT 84112; janis.weis@path.utah.edu.
University of Utah · USUniversity of Puget Sound · USUniversity of Vermont · US

Funding

MOLECULAR GENETICS OF LYME ARTHRITIS SUSCEPTIBILITYR01AR043521 · NIAMS · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 1994 to 2024
$9.4M
BORRELIA BURGDORFERI MITOGEN IN DEVELOPMENT OF ARTHRITISR01AI032223 · NIAID · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 1993 to 2023
$7.8M
Training Program in Microbial PathogenesisT32AI055434 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MULVEY, MATTHEW A, PLANELLES, VICENTE · 2004 to 2025
$6.0M
Borrelia Burgdorferi Mitogen in Development of ArthritisR56AI032223 · NIAID · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 2013 to 2013
$350k
NCI NIH HHS P30 CA04201NIAID NIH HHS AI32223NIAID NIH HHS R01 AI032223NIAID NIH HHS R56 AI032223NIAID NIH HHS T32 AI055434NIAID NIH HHS T32AI055434NIAMS NIH HHS AR43521NIAMS NIH HHS R01 AR043521
6 · The paper itself

Abstract

The lysosomal enzyme β-glucuronidase (Gusb) is a key regulator of Lyme-associated and K/B×N-induced arthritis severity. The luminal enzymes present in lysosomes provide essential catabolic functions for the homeostatic degradation of a variety of macromolecules. In addition to this essential catabolic function, lysosomes play important roles in the inflammatory response following infection. Secretory lysosomes and related vesicles can participate in the inflammatory response through fusion with the plasma membrane and release of bioactive contents into the extracellular milieu. In this study, we show that GUSB hypomorphism potentiates lysosomal exocytosis following inflammatory stimulation. This leads to elevated secretion of lysosomal contents, including glycosaminoglycans, lysosomal hydrolases, and matrix metalloproteinase 9, a known modulator of Lyme arthritis severity. This mechanistic insight led us to test the efficacy of rapamycin, a drug known to suppress lysosomal exocytosis. Both Lyme and K/B×N-associated arthritis were suppressed by this treatment concurrent with reduced lysosomal release.

Indexed as

AnimalsCell MembraneDisease Models, AnimalExocytosisGlucuronidaseImmunosuppressive AgentsLyme DiseaseLysosomal-Associated Membrane Protein 1LysosomesMacrophagesMatrix Metalloproteinase 9MiceMice, KnockoutModels, BiologicalProtein TransportSirolimusGlucuronidaseImmunosuppressive AgentsLysosomal-Associated Membrane Protein 1Matrix Metalloproteinase 9Sirolimus

Identifiers

PMID26170381
PMCPMC4530054
OpenAlexW2116758845

What OpenQuestion holds

Textmetadata
LicenceTDM
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.