Evidence map›Paper›PMID 28141831›Full record

ArticlePloS one2017

B7-H3 Augments Inflammatory Responses and Exacerbates Brain Damage via Amplifying NF-κB p65 and MAPK p38 Activation during Experimental Pneumococcal Meningitis.

Xuqin Chen, Yan Li, Siobhan Blankson, Min Liu, Danping Huang, H Paul Redmond, Jing Huang, Jiang Huai Wang, Jian Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  4. Potential value of B7-H3 in sepsis diagnosis and prognosis: A Mendelian randomization study.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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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

9 authors at 3 institutions in 2 countries.

Xuqin ChenDepartment of Neurology, Children's Hospital of Soochow University, Suzhou, China.
Yan LiDepartment of Neurology, Children's Hospital of Soochow University, Suzhou, China.
Siobhan BlanksonDepartment of Academic Surgery, University College Cork, Cork University Hospital, Cork, Ireland.
Min LiuDepartment of Neurology, Children's Hospital of Soochow University, Suzhou, China.
Danping HuangDepartment of Neurology, Children's Hospital of Soochow University, Suzhou, China.
H Paul RedmondDepartment of Academic Surgery, University College Cork, Cork University Hospital, Cork, Ireland.
Jing HuangDepartment of Neurology, Children's Hospital of Soochow University, Suzhou, China.
Jiang Huai WangDepartment of Academic Surgery, University College Cork, Cork University Hospital, Cork, Ireland.
Jian WangPediatric Research Institute of Soochow University, Suzhou, China.
Soochow University · CNUniversity College Cork · IECork University Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The costimulatory protein B7-H3 has been shown to play a contributory role in the development and progression of experimental pneumococcal meningitis by augmentation of the innate immunity-associated inflammatory response via a TLR2-dependent manner. This study aimed to clarify the component(s) of TLR2-mediated signal transduction pathways responsible for B7-H3-augmented inflammatory response and subsequent brain damage during experimental pneumococcal meningitis. Administration of B7-H3 did not augment expression of TLR2 and other TLR2 upstream components, but led to an enhanced formation of MyD88-IRAK immunocomplex in the brain of S. pneumoniae-infected mice. Furthermore, B7-H3 substantially augmented S. pneumoniae-induced activation of TLR2 downstream NF-κB p65 and MAPK p38 pathways in the brain of S. pneumoniae-infected mice. Notably, blockage of NF-κB p65 and/or MAPK p38 with their specific inhibitors strongly attenuated B7-H3-amplified inflammatory response with significantly reduced proinflammatory cytokine and chemokine production, and markedly ameliorated B7-H3-exacerbated disruption of blood-brain barrier and severity of disease status in S. pneumoniae-infected mice. These results indicate that targeting NF-κB p65 and/or MAPK p38 may represent a promising therapeutic option for amelioration of overwhelming inflammatory response-associated brain injury frequently observed during pneumococcal meningitis.

Indexed as

Disease ProgressionAnimalsB7 AntigensBlood-Brain BarrierBrainBrain InjuriesEnzyme ActivationInflammationInterleukin-1 Receptor-Associated KinasesMaleMembrane GlycoproteinsMeningitis, PneumococcalMice, Inbred BALB CMyeloid Differentiation Factor 88p38 Mitogen-Activated Protein KinasesPhosphorylationB7 AntigensCd276 protein, mouseInterleukin-1 Receptor-Associated KinasesIrak1 protein, mouseMembrane GlycoproteinsMyeloid Differentiation Factor 88p38 Mitogen-Activated Protein KinasesReceptors, Interleukin-1RNA, MessengerTIRAP protein, mouseTNF Receptor-Associated Factor 6Toll-Like Receptor 2Transcription Factor RelA

Identifiers

PMID28141831
PMCPMC5283727
OpenAlexW2583286474

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.