Scholarlink

Background <p>Asthma prevalence has been increasing, particularly among children and in populations transitioning to Western lifestyle. According to the hygiene hypothesis, early-life exposure to microorganisms may protect against asthma and other allergic conditions. Previous studies demonstrated that <i>Saccharomyces cerevisiae</i> UFMG A-905 reduce bronchial hyperresponsiveness, airway and lung inflammation, and restore IL-10 and IFN-γ. However, the underlying mechanisms remain unclear.</p> Objective <p>To investigate the potential pathways by which <i>S. cerevisiae</i> UFMG A-905 modulates asthma.</p> Materials and methods <p>Wild-type and <i>Il17a⁻/⁻</i> mice were treated daily with live yeast or its supernatant (postbiotic) by oral gavage, starting ten days before OVA sensitization and maintained during sensitization and challenge. Control groups received saline. Lung tissues were analyzed by flow cytometry to assess dendritic cells and regulatory T cells. Gene expression of TLR-9, NLRP3, Dectin-1, and Mincle was quantified by qPCR. Short-, medium-, and long-chain fatty acids were measured in feces using gas chromatography, while gut cytokine were evaluated by ELISA.</p> Results <p>Treatment with <i>S. cerevisiae</i> UFMG A-905 led to an increase in CD11c⁺MHCII⁺CD11b⁺CD103⁻ dendritic cells, regulatory T cells (CD4⁺CD25⁺FOXP3⁺), and NLRP3 gene expression in the lung, and the fecal levels of dihomo-γ-linolenic acid. Neither gut cytokines nor OVA specific IgE were affected, and the supernatant did not significantly alter cell counts. The beneficial effects were partially dependent on IL-17A.</p> Conclusion <p>The effects observed with <i>S. cerevisiae</i> UFMG A-905 correlated with modulation of Th17, dendritic-cell and regulatory T-cell responses, upregulation of NLRP3, and increased fatty acid production, suggesting gut–lung axis involvement.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Saccharomyces cerevisiae UFMG A-905 acts in an animal model of asthma by modulating Th17/Treg responses and increasing fatty acid production

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月10日

查看全文
  • Vanessa Maciel Braulio da Fonseca,
  • Camila Mira Sandy,
  • Camila Carla Guimarães,
  • Alceu Afonso Jordão Junior,
  • Jacques Robert Nicoli,
  • Flaviano Santos Martins,
  • Marcos Carvalho Borges

摘要

Background

Asthma prevalence has been increasing, particularly among children and in populations transitioning to Western lifestyle. According to the hygiene hypothesis, early-life exposure to microorganisms may protect against asthma and other allergic conditions. Previous studies demonstrated that Saccharomyces cerevisiae UFMG A-905 reduce bronchial hyperresponsiveness, airway and lung inflammation, and restore IL-10 and IFN-γ. However, the underlying mechanisms remain unclear.

Objective

To investigate the potential pathways by which S. cerevisiae UFMG A-905 modulates asthma.

Materials and methods

Wild-type and Il17a⁻/⁻ mice were treated daily with live yeast or its supernatant (postbiotic) by oral gavage, starting ten days before OVA sensitization and maintained during sensitization and challenge. Control groups received saline. Lung tissues were analyzed by flow cytometry to assess dendritic cells and regulatory T cells. Gene expression of TLR-9, NLRP3, Dectin-1, and Mincle was quantified by qPCR. Short-, medium-, and long-chain fatty acids were measured in feces using gas chromatography, while gut cytokine were evaluated by ELISA.

Results

Treatment with S. cerevisiae UFMG A-905 led to an increase in CD11c⁺MHCII⁺CD11b⁺CD103⁻ dendritic cells, regulatory T cells (CD4⁺CD25⁺FOXP3⁺), and NLRP3 gene expression in the lung, and the fecal levels of dihomo-γ-linolenic acid. Neither gut cytokines nor OVA specific IgE were affected, and the supernatant did not significantly alter cell counts. The beneficial effects were partially dependent on IL-17A.

Conclusion

The effects observed with S. cerevisiae UFMG A-905 correlated with modulation of Th17, dendritic-cell and regulatory T-cell responses, upregulation of NLRP3, and increased fatty acid production, suggesting gut–lung axis involvement.