Evidence map›Paper›PMID 27364893›Full record

ArticleExperimental & molecular medicine2016

The role of autophagy in allergic inflammation: a new target for severe asthma.

Jing-Nan Liu, Dong-Hyeon Suh, Hoang Kim Tu Trinh, Yong-Joon Chwae, Hae-Sim Park, Yoo Seob Shin

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
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  6. Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025
    Review
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  12. Food science & nutrition · 2025
    Article
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10 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Jing-Nan LiuDepartment of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Dong-Hyeon SuhDepartment of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Hoang Kim Tu TrinhDepartment of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Yong-Joon ChwaeDepartment of Microbiology, Ajou University School of Medicine, Suwon, Korea.
Hae-Sim ParkDepartment of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Yoo Seob ShinDepartment of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Ajou University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy has been investigated for its involvement in inflammatory diseases, but its role in asthma has been little studied. This study aimed to explore the possible role of autophagy and its therapeutic potential in severe allergic asthma. BALB/c mice were sensitized with ovalbumin (OVA) on days 0 and 14, followed by primary OVA challenge on days 28-30. The mice received a secondary 1 or 2% OVA challenge on days 44-46. After the final OVA challenge, the mice were assessed for airway responsiveness (AHR), cell composition and cytokine levels in bronchoalveolar lavage fluid (BALF). LC3 expression in lung tissue was measured by western blot and immunofluorescence staining. Autophagosomes were detected by electron microscopy. 3-Methyladenine (3-MA) treatment and Atg5 knockdown were applied to investigate the potential role of autophagy in allergic asthma mice. AHR, inflammation in BALF and LC3 expression in lung tissue were significantly increased in the 2% OVA-challenged mice compared with the 1% OVA-challenged mice (P<0.05). In addition, eosinophils showed prominent formation of autophagosomes and increased LC3 expression compared with other inflammatory cells in BALF and lung tissue. After autophagy was inhibited by 3-MA and Atg5 shRNA treatment, AHR, eosinophilia, interleukin (IL)-5 levels in BALF and histological inflammatory findings were much improved. Finally, treatment with an anti-IL-5 antibody considerably reduced LC3 II expression in lung homogenates. Our findings suggest that autophagy is closely correlated with the severity of asthma through eosinophilic inflammation, and its modulation may provide novel therapeutic approaches for severe allergic asthma.

Indexed as

AutophagyAnimalsAsthmaBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalEosinophilsFemaleInflammationLungMice, Inbred BALB CMicrotubule-Associated ProteinsOvalbuminCytokinesMap1lc3b protein, mouseMicrotubule-Associated ProteinsOvalbumin

Identifiers

PMID27364893
PMCPMC4973311
OpenAlexW2474534968

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.