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Resveratrol reduces inflammatory responses in peripheral blood mononuclear cells from patients with severe asthma.

Created on 13 Oct 2026

Authors

Wanessa Maria Dos Santos, Dayana Procópia Macies, Lara Cristina Dos Santos Teodoro, Mirella Castro Queiroz, Jefferson Correia Manso, Beatriz Sodré Matos, Anna Luiza Dos Anjos Oliveiras, Isabella de Oliveira Ferrato de Sousa, Maria Helena de Castro Silva, Daniel Hugo Winter, Leandro de Resende Yamamoto, Alexandre Paula Rogerio

Published in

Immunopharmacology and immunotoxicology. Pages 1-7. Oct 12, 2026. Epub Oct 12, 2026.

Abstract

Severe asthma is a chronic inflammatory airway disease frequently associated with neutrophilic inflammation, corticosteroid resistance, and persistent activation of pro-inflammatory signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs).
This study aimed to investigate the effects of resveratrol on inflammatory responses in peripheral blood mononuclear cells (PBMCs) obtained from healthy subjects and patients with severe asthma.
PBMCs were stimulated with lipopolysaccharide (LPS; 1 µg/mL) for 24 h in the presence or absence of resveratrol (10-4-10-8 M). Cell viability was assessed using the MTT assay, cytokine levels (IL-6, IL-8, and IL-10) were measured by ELISA, and intracellular signaling pathways (NF-κB, ERK1/2, and p38 MAPK) were evaluated by flow cytometry.
Resveratrol did not affect cell viability and significantly reduced IL-6 and IL-8 production in a dose-dependent manner in LPS-stimulated PBMCs, without altering IL-10 levels. Additionally, resveratrol attenuated the phosphorylation of NF-κB, ERK1/2, and p38 MAPK in both monocytes and lymphocytes from healthy individuals and patients with severe asthma.
Resveratrol exerts significant anti-inflammatory effects in human PBMCs by modulating cytokine production and key intracellular signaling pathways associated with severe asthma, suggesting its potential as a complementary therapeutic strategy.

PMID:
42865112
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.

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