Evidence map›Paper›PMID 36426399›Full record

ArticleAllergy, asthma & immunology research2022

Metabolism Characteristics of

Jiaying Luo, Huian Chen, Qiyong Zhang, Xinyun Huang, Xu Qin, Jing Li, Siyi Chen, Yongxin Xiao, Lihong Sun, Baoqing Sun

Open access · diamondAbstract read
In one paragraph

Article in Allergy, asthma & immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  4. Effect of PMScientific reports · 2025
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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 1 country.

Jiaying Luo *State Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0003-1130-3288
Huian Chen *State Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0003-3786-9191
Qiyong ZhangThe Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xinyun HuangState Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xu QinState Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-0655-5547
Jing LiInstitute of Integrated Traditional Chinese and Western Medicine, Guangzhou Medical University, Guangzhou, China.
Siyi ChenState Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-2610-8912
Yongxin XiaoState Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-9768-1783
Lihong SunState Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. sunlihong9797@126.com.ORCID https://orcid.org/0000-0002-0495-8991
Baoqing SunState Key Lab of Respiratory Disease, National Clinical Research Center of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. sunbaoqing@vip.163.com.ORCID https://orcid.org/0000-0002-1671-0723
First Affiliated Hospital of Guangzhou Medical University · CNGuangzhou University of Chinese Medicine · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeStudies have shown that

methodsWe divided the subjects into the asthma, Mp infection, asthma combined with Mp infection and healthy groups. Patients' peripheral blood was collected for metabolic and interaction analysis. Cytokine levels were measured via serum and exhaled breath condensate (EBC).

resultsA total of 150 participating subjects were divided into four groups after exclusion. We found out that there were different metabolic pathways between the healthy and disease groups. The major pathways of both asthma and asthma combined with Mp infection were valine, leucine and isoleucine biosynthesis; malate-aspartate shuttle was the main differential pathway for Mp infection. Moreover, even though three disease groups involved 81 metabolites at the same time, compared with asthma combined with Mp infection, 2 single disease groups still involved different amino acid pathways (phenylalanine, tyrosine and tryptophan biosynthesis; valine, leucine and isoleucine biosynthesis). Interaction analysis showed that Mp infection in asthmatic patients not only activated cytokines, but also activated Toll-like receptors (TLRs) 2 and 6. Finally, the levels of interleukin (IL)-4, IL-8, IL-13 and tumor necrosis factor-α in EBC with asthma combined with Mp infection were significantly higher than the 2 single disease groups.

conclusionsMp infection in asthmatic children can cause changes in the levels of various amino acids in the body, which were enriched in the pathways such as valine, leucine and isoleucine biosynthesis. Palmitic acid can activate TLR2, and iloprost reduces IL-10 levels, ultimately leading to the increased airway inflammation.

Indexed as

AsthmacytokinesmetabolomicsMycoplasma pneumoniaeToll-like receptors

Identifiers

PMID36426399
PMCPMC9709688
OpenAlexW4310332680

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.