Evidence map›Paper›PMID 34405339›Full record

ArticleInflammopharmacology2021

Anti-inflammatory actions of aspirin-triggered resolvin D1 (AT-RvD1) in bronchial epithelial cells infected with Cryptococcus neoformans.

Bruno Sada Salerno, Aline Beatriz Mahler Pereira, Henrique Ismarsi de Souza, Mario Leon Silva-Vergara, Bruce David Levy, Alexandre Paula Rogerio

Abstract read
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In one paragraph

Article in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Aspirin Combined with Antifungal Drugs SuppressesJournal of microbiology and biotechnology · 2025
    Article
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 2 institutions in 2 countries.

Bruno Sada SalernoLaboratory of Experimental Immunopharmacology, Department of Clinical Medicine, Institute of Health Sciences, Federal University of Triangulo Mineiro, Street Vigário Carlos 162, Uberaba, MG, 38025-380, Brazil.
Aline Beatriz Mahler PereiraLaboratory of Experimental Immunopharmacology, Department of Clinical Medicine, Institute of Health Sciences, Federal University of Triangulo Mineiro, Street Vigário Carlos 162, Uberaba, MG, 38025-380, Brazil.
Henrique Ismarsi de SouzaLaboratory of Experimental Immunopharmacology, Department of Clinical Medicine, Institute of Health Sciences, Federal University of Triangulo Mineiro, Street Vigário Carlos 162, Uberaba, MG, 38025-380, Brazil.
Mario Leon Silva-VergaraLaboratory of Mycology, Department of Clinical Medicine, Institute of Health Sciences, Federal University of Triangulo Mineiro, Uberaba, MG, Brazil.
Bruce David LevyPulmonary and Critical Care Medicine Division, Department of Internal Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Alexandre Paula RogerioLaboratory of Experimental Immunopharmacology, Department of Clinical Medicine, Institute of Health Sciences, Federal University of Triangulo Mineiro, Street Vigário Carlos 162, Uberaba, MG, 38025-380, Brazil. alexandre.rogerio@uftm.edu.br.ORCID http://orcid.org/0000-0001-5913-3703
Universidade Federal do Triângulo Mineiro · BRBrigham and Women's Hospital · US

Funding

CAPES 001CNPq 475349/2010-5FAPEMIG APQ 01631/11 and APQ-01873-14
6 · The paper itself

Abstract

backgroundThe interaction of Cryptococcus neoformans with airway epithelial cells is crucial for the establishment of cryptococcosis. Aspirin-triggered-resolvin D1 (AT-RvD1) is a lipid mediator produced during the resolution of inflammation and demonstrates anti-inflammatory and pro-resolution effects in several inflammatory experimental models including in the airways.

methodHere, we evaluated the effects of AT-RvD1 (1, 10 or 100 nM) on human bronchial epithelial cells (BEAS-2B) stimulated with C. neoformans (1, 10 or 100 multiplicities of infection; MOI).

resultsAfter 24 h, C. neoformans (all MOI) demonstrated no cytotoxic effects and increased IL-8 production on BEAS-2B cells when compared to controls. In addition, C. neoformans (MOI 100) increased the concentration of IL-6, but not of IL-10. AT-RvD1 (100 nM) significantly reduced the concentration of IL-8 and IL-6 and increased IL-10 production in C. neoformans-stimulated BEAS-2B cells. C. neoformans increased the phosphorylation of NF-κB and ERK1/2, and ALX/FPR2 expression. AT-RvD1 reduced the activation of NF-kB without altering the ERK1/2 and ALX/FPR2 expression. The anti-inflammatory effects of AT-RvD1 were dependent on the ALX/FPR2, once its antagonist (BOC2) reversed its anti-inflammatory effects. No alteration on the fungal burden as well as interactions with BEAS-2B cells was observed by AT-RvD1.

conclusionAT-RvD1 demonstrated significant anti-inflammatory effects in bronchial epithelial cells infected with C. neoformans without affecting the development of C. neoformans infection in the airways.

trial registrationNot applicable.

Indexed as

Anti-Inflammatory AgentsBronchiCell LineCryptococcosisCryptococcus neoformansDocosahexaenoic AcidsDose-Response Relationship, DrugEpithelial CellsHumansInflammationAnti-Inflammatory AgentsDocosahexaenoic Acidsresolvin D1AT-RvD1Bronchial epithelial cellsCryptococcus neoformansLipid mediator

Identifiers

PMID34405339
OpenAlexW3194830163

What OpenQuestion holds

Textmetadata
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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.