Evidence map›Paper›PMID 29695898›Full record

ArticleInternational journal of chronic obstructive pulmonary disease

Critical regulation of inflammation via class A scavenger receptor.

Liang Xie, Qingmin Li, Ran Dong, Kaishun Zhao, Yun Feng, Zhiyao Bao, Min Zhou

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of chronic obstructive pulmonary disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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

7 authors at 4 institutions in 1 country.

Liang Xie *Department of Pulmonary and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Qingmin Li *Department of Cardiology, Henan Provincial Peoples Hospital, Zhengzhou, China.
Ran Dong *Department of Respiratory Medicine, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Kaishun ZhaoDepartment of Respiratory Medicine, Jiading Central Hospital, Shanghai, China.
Yun FengDepartment of Pulmonary and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Zhiyao BaoDepartment of Pulmonary and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Min ZhouDepartment of Pulmonary and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Ruijin Hospital · CNHenan Provincial People's Hospital · CNJiading District Central Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammation is an important cause of COPD. Alveolar macrophages are the major innate immune cells that have an important role in COPD pathology. Class A scavenger receptor (SR-A) is a pattern recognition receptor expressed on macrophages. This study investigates the role of SR-A in COPD progression via regulation of inflammation. PATIENTS AND

methodsSR-A expression in COPD patients and control subjects (smokers and nonsmokers without COPD) was measured by immunohistochemistry, immunofluorescence, and real-time PCR. The cytokine levels in BAL were measured by enzyme-linked immunosorbent assay. To further prove our hypothesis, we treated RAW264.7 cells that overexpress SR-A with lipopolysaccharides, poly(I:C), cigarette smoke extract, and H1N1 influenza separated from patients for 24 h and examined the levels of inflammatory cytokines.

resultsIn both groups, COPD and smokers without COPD, SR-A expression level was upregulated in alveolar macrophages. SR-A mRNA level was positively correlated with inflammatory cytokines and negatively correlated with FEV

conclusionSR-A could increase inflammation stimulated by cigarette smoke extracts, bacteria, and virus, leading to long-term inflammation in COPD, and thus might be used as a new therapeutic target for COPD treatment.

Indexed as

AgedAnimalsCase-Control StudiesCytokinesFemaleForced Expiratory VolumeHost-Pathogen InteractionsHumansInflammation MediatorsInfluenza A Virus, H1N1 SubtypeLipopolysaccharidesLungMacrophages, AlveolarMaleMiceMiddle AgedCytokinesInflammation Mediatorslipopolysaccharide, E coli O55-B5LipopolysaccharidesPoly I-CScavenger Receptors, Class ASmokechronic obstructive pulmonary diseasecigarette smoke extractclass A scavenger receptorH1N1 influenzainflammationlipopolysaccharidespoly(I:C)

Identifiers

PMID29695898
PMCPMC5905844
OpenAlexW2798067132

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.