Evidence map›Paper›PMID 23611998›Full record

ArticleInvestigative ophthalmology & visual science2013

TREM-2 promotes host resistance against Pseudomonas aeruginosa infection by suppressing corneal inflammation via a PI3K/Akt signaling pathway.

Mingxia Sun, Min Zhu, Kang Chen, Xinxin Nie, Qiuchan Deng, Linda D Hazlett, Yongjian Wu, Meiyu Li, Minhao Wu, Xi Huang

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 60 citations in OpenAlex.

  1. TREM2 drives monocyte-derived macrophage responses tobioRxiv : the preprint server for biology · 2026
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  13. Paeonol Interferes With Quorum-Sensing inFrontiers in immunology · 2022
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  15. Review
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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

10 authors at 3 institutions in 2 countries.

Mingxia SunDepartment of Immunology, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Min Zhu
Kang Chen
Xinxin Nie
Qiuchan Deng
Linda D Hazlett
Yongjian Wu
Meiyu Li
Minhao Wu
Xi Huang
Sun Yat-sen University · CNWayne State University · USZhongshan Ophthalmic Center, Sun Yat-sen University

Funding

VISION RESEARCH--COREP30EY004068 · NEI · WAYNE STATE UNIVERSITY · PI LINDA D HAZLETT · 1985 to 2026
$13.2M
Role of Toll-Like Receptors in Bacterial KeratitisR01EY016058 · NEI · WAYNE STATE UNIVERSITY · PI HAZLETT, LINDA D · 2005 to 2023
$6.0M
Role of Triggering Receptors Expressed on Myeloid Cells in Bacterial KeratitisR01EY019021 · NEI · WAYNE STATE UNIVERSITY · PI HUANG, XI · 2008 to 2011
$1.3M
NEI NIH HHS P30 EY004068NEI NIH HHS P30 EY04068NEI NIH HHS R01 EY016058NEI NIH HHS R01 EY019021
6 · The paper itself

Abstract

purposeTo explore the role of triggering receptor expressed on myeloid cells 2 (TREM-2) in Pseudomonas aeruginosa (PA) keratitis.

methodsBALB/c mice were routinely infected with PA and evaluated at various postinfection time points for corneal expression of TREM-2, by real-time PCR, Western blot, and flow cytometry. Next, BALB/c and C57BL/6 mice were respectively treated with TREM-2 siRNA or agonistic anti-TREM-2 antibody, to determine the role of TREM-2 in PA keratitis. Bacterial load and neutrophil infiltration were tested by plate count and myeloperoxidase assay, respectively. Th1-/Th2-type and proinflammatory cytokine expression were tested by real-time PCR and ELISA after in vivo and in vitro silencing of TREM-2. Moreover, phosphorylated Akt levels were tested by Western blot in murine macrophages after treatment with agonistic anti-TREM-2 antibody. mRNA levels of proinflammatory cytokines were examined in murine macrophages after TREM-2 activation and lipopolysaccharide stimulation, following pretreatment with inhibitors for PI3K or Akt, to determine whether PI3K/Akt is required in TREM-2-mediated immune modulation. In addition, BALB/c mice were treated with wortmannin and analyzed for bacterial load and proinflammatory cytokine expression.

resultsTREM-2 expression was elevated in the infected BALB/c corneas at 3 or 5 days postinfection. Silencing of TREM-2 accelerated disease progression by enhancing bacterial load and corneal inflammation, whereas activation of TREM-2 promoted host resistance to PA keratitis. PI3K/Akt signaling is required in the TREM-2-mediated immune modulation, and inhibition of PI3K resulted in worsened disease after PA corneal infection.

conclusionsTREM-2 promoted host resistance to PA infection by suppressing corneal inflammation via activation of the PI3K/Akt pathway.

Indexed as

Immunity, InnateAnimalsBlotting, WesternCells, CulturedColony Count, MicrobialCytokinesEnzyme-Linked Immunosorbent AssayEye Infections, BacterialFlow CytometryKeratitisMacrophagesMembrane GlycoproteinsMiceMice, Inbred BALB CMice, Inbred C57BLNeutrophilsCytokinesMembrane GlycoproteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, ImmunologicRNA, Small InterferingTrem2 protein, mousebacteriacorneacytokinesinflammation

Identifiers

PMID23611998
PMCPMC3658264
OpenAlexW2089938014

What OpenQuestion holds

Textmetadata
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.