Evidence map›Paper›PMID 25905462›Full record

ArticlePloS one2015

Thalidomide inhibits alternative activation of macrophages in vivo and in vitro: a potential mechanism of anti-asthmatic effect of thalidomide.

Hyun Seung Lee, Hyouk-Soo Kwon, Da-Eun Park, Yeon Duk Woo, Hye Young Kim, Hang-Rae Kim, Sang-Heon Cho, Kyung-Up Min, Hye-Ryun Kang, Yoon-Seok Chang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 23 citations in OpenAlex.

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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.

Hyun Seung LeeInstitute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea.
Hyouk-Soo KwonInstitute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea; Department of Internal medicine, Seoul National University College of Medicine, Seoul, Korea.
Da-Eun ParkInstitute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea.
Yeon Duk WooDepartment of Medical Science, Seoul National University College of Medicine, Seoul, Korea.
Hye Young KimDepartment of Medical Science, Seoul National University College of Medicine, Seoul, Korea.
Hang-Rae KimDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Korea.
Sang-Heon ChoInstitute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea; Department of Internal medicine, Seoul National University College of Medicine, Seoul, Korea.
Kyung-Up MinInstitute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea; Department of Internal medicine, Seoul National University College of Medicine, Seoul, Korea.
Hye-Ryun KangInstitute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea; Department of Internal medicine, Seoul National University College of Medicine, Seoul, Korea.
Yoon-Seok ChangDepartment of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Gyeonggi-do, Korea.
Seoul National University · KRSeoul National University Hospital · KRSeoul National University Bundang Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThalidomide is known to have anti-inflammatory and immunomodulatory actions. However, the effect and the anti-asthmatic mechanism of thalidomide in the pathogenesis of asthmatic airways are not fully understood.

objectiveThis study is designed to determine the effect and the potential mechanism of thalidomide in the pathogenesis of asthmatic airways using animal model of allergic asthma.

methodsSix-week-old female BALB/C mice were sensitized with alum plus ovalbumin (OVA) and were exposed to OVA via intranasal route for 3 days for challenge. Thalidomide 200 mg/kg was given via gavage twice a day from a day before the challenge and airway hyperresponsivenss (AHR), airway inflammatory cells, and cytokines in bronchoalveolar lavage fluids (BALF) were evaluated. The expression levels of pro-inflammatory cytokines and other mediators were evaluated using ELISA, real time (RT)-qPCR, and flow cytometry. CRL-2456, alveolar macrophage cell line, was used to test the direct effect of thalidomide on the activation of macrophages in vitro.

resultsThe mice with thalidomide treatment showed significantly reduced levels of allergen-induced BALF and lung inflammation, AHR, and the expression of a number of pro-inflammatory cytokines and mediators including Th2 related, IL-17 cytokines, and altered levels of allergen-specific IgG1/IgG2a. Of interesting note, thalidomide treatment significantly reduced expression levels of allergen- or Th2 cytokine-stimulated alternative activation of macrophages in vivo and in vitro.

conclusionThese studies highlight a potential use of thalidomide in the treatment of allergic diseases including asthma. This study further identified a novel inhibitory effect of thalidomide on alternative activation of macrophages as a potential mechanism of anti-asthmatic effect of thalidomide.

Indexed as

AllergensAlum CompoundsAnimalsAnti-Asthmatic AgentsAnti-Inflammatory AgentsAsthmaBronchial HyperreactivityBronchoalveolar Lavage FluidDisease Models, AnimalFemaleImmunoglobulin GInflammationInterleukin-17Macrophages, AlveolarMiceMice, Inbred BALB CAllergensAlum CompoundsAnti-Asthmatic AgentsAnti-Inflammatory AgentsIL17A protein, humanImmunoglobulin GInterleukin-17Ovalbuminovalbumin-alumThalidomide

Identifiers

PMID25905462
PMCPMC4408009
OpenAlexW2075302307

What OpenQuestion holds

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LicenceCC BY
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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.