Evidence map›Paper›PMID 30021797›Full record

ArticleThe Journal of experimental medicine2018

LPS inactivation by a host lipase allows lung epithelial cell sensitization for allergic asthma.

Guojun Qian, Wei Jiang, Benkun Zou, Jintao Feng, Xiaofang Cheng, Jie Gu, Tianqing Chu, Chen Niu, Rui He, Yiwei Chu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 68 citations in OpenAlex.

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  20. The lung-gut crosstalk in respiratory and inflammatory bowel disease.Frontiers in cellular and infection microbiology · 2023
    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

11 authors at 3 institutions in 1 country.

Guojun QianDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Wei JiangDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Benkun ZouDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Jintao FengDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Xiaofang ChengDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Jie GuDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Tianqing ChuDepartment of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Chen NiuDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Rui HeDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.ORCID 0000-0001-5288-9786
Yiwei ChuDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.ORCID 0000-0002-5035-1111
Mingfang LuDepartment of Immunology, MOE & MOH Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China mingfanglu@fudan.edu.cn.ORCID 0000-0002-8612-3444
Fudan University · CNShanghai Jiao Tong University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic asthma is a chronic inflammatory disease primarily mediated by Th2 immune mechanisms. Numerous studies have suggested that early life exposure to lipopolysaccharide (LPS) is negatively associated with allergic asthma. One proposed mechanism invokes desensitization of lung epithelial cells by LPS. We report here that acyloxyacyl hydrolase (AOAH), a host lipase that degrades and inactivates LPS, renders mice more susceptible to house dust mite (HDM)-induced allergic asthma. Lung epithelial cells from

Indexed as

AnimalsAsthmaCarboxylic Ester HydrolasesDendritic CellsDisease Models, AnimalEpithelial CellsLipaseLipopolysaccharidesLungMiceMice, KnockoutTh2 Cellsacyloxyacyl hydrolaseCarboxylic Ester HydrolasesLipaseLipopolysaccharides

Identifiers

PMID30021797
PMCPMC6122967
OpenAlexW2884180544

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.