Evidence map›Paper›PMID 34311579›Full record

ArticlemBio2021

CCR2 Signaling Promotes Brain Infiltration of Inflammatory Monocytes and Contributes to Neuropathology during Cryptococcal Meningoencephalitis.

Jintao Xu, Anutosh Ganguly, Jessica Zhao, Michel Ivey, Rafael Lopez, John J Osterholzer, Clifford S Cho, Michal A Olszewski

Open access · goldAbstract read
In one paragraph

Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Jintao XuResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
Anutosh GangulyResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
Jessica ZhaoResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
Michel IveyResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
Rafael LopezResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
John J OsterholzerResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
Clifford S ChoResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
Michal A OlszewskiResearch Service, Ann Arbor VA Health System, Department of Veterans Affairs Health System, Ann Arbor, Michigan, USA.
VA Ann Arbor Healthcare System · USUniversity of Michigan · US

Funding

Modulation of Pulmonary Defenses in Pathobiology of Chronic InfectionsI01BX000656 · VA · VETERANS HEALTH ADMINISTRATION · PI OLSZEWSKI, MICHAL A · 2011 to 2025
–
Re-engineering the tumor draining lymph node to achieve memory T cell-based adoptive immunotherapyI01BX001619 · VA · WM S. MIDDLETON MEMORIAL VETERANS HOSP · PI CHO, CLIFFORD · 2014 to 2022
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Advancing Non-Invasive Diagnostics and Treatments of Deployment-Related Chronic Lung Disease in Gulf War VeteransI01BX004740 · VA · VETERANS HEALTH ADMINISTRATION · PI JOHN OSTERHOLZER · 2020 to 2026
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BLR&D Research Career Scientist Award ApplicationIK6BX003615 · VA · VETERANS HEALTH ADMINISTRATION · PI OLSZEWSKI, MICHAL A · 2017 to 2021
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BLRD VA I01 BX000656BLRD VA I01 BX001619BLRD VA I01 BX004740BLRD VA IK6 BX003615
6 · The paper itself

Abstract

Cryptococcal meningoencephalitis (CM) is a leading cause of central nervous system (CNS) infection-related mortality worldwide, with surviving patients often developing neurological deficiencies. While CNS inflammation has been implicated in the pathogenesis of CM, little is known about the relative contribution of the specific inflammatory/immune pathways to CNS pathology versus fungal clearance. Increased cerebrospinal fluid level of C-C chemokine receptor 2 (CCR2) ligand CCL2 is associated with disease deterioration in patients with CM. Using a murine model, we investigated the role of the CCR2 pathway in the development of CNS inflammation and pathology during CM. We found that CCR2-deficient mice exhibited improved 28-day survival and alleviated neurological disease scores despite a brain fungal burden higher than that of the WT mice. Reduced CM pathology in CCR2-deficient mice was accompanied by markedly decreased neuronal cell death around cryptococcal microcysts and restored expression of genes involved in neurotransmission, connectivity, and neuronal cell structure in the brains. Results show that CCR2 axis is the major pathway recruiting CD45

Indexed as

AnimalsBrainCryptococcosisCryptococcusFemaleInflammationMaleMeningoencephalitisMiceMice, Inbred C57BLMice, KnockoutMonocytesReceptors, CCR2Signal TransductionCcr2 protein, mouseReceptors, CCR2CCR2central nervous system infectionscryptococcal meningoencephalitisimmunopathogenesisinflammatory monocyte

Identifiers

PMID34311579
PMCPMC8406332
OpenAlexW3183295235

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.