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. 2026 Jan 10;26:138. doi: 10.1186/s12866-025-04660-7

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

Vanessa Maciel Braulio da Fonseca 1, Camila Mira Sandy 1, Camila Carla Guimarães 1, Alceu Afonso Jordão Junior 2, Jacques Robert Nicoli 3, Flaviano Santos Martins 3, Marcos Carvalho Borges 1,✉
PMCID: PMC12918630  PMID: 41519696

Abstract

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.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12866-025-04660-7.

Keywords: Probiotics, Asthma, Prevention, S. cerevisiae UFMG A-905

Introduction

Asthma is a chronic disease and a global health problem with significant impacts on quality of life and economic burden, particularly in countries that have adopted a Western lifestyle and became more urbanized [1, 2]. This heterogeneous disease affects both children and adults and is characterized by airway hyperresponsiveness (AHR) and inflammation, bronchial remodeling, and variable airflow limitation, which can be reversible spontaneously or with treatment [3].

Several factors contribute to asthma development and severity, including obesity, sex, immune dysregulation, genetic predisposition, environmental and occupational exposure, tobacco smoke, diet, infections, and limited exposure to beneficial microbes [3]. Additionally, some studies demonstrated the importance of the microbiome and the complex interactions between the gut and lung [4, 5]. The mechanisms involved in the gut-lung axis are not well understood, but dendritic cells (DCs), pattern recognition receptors (PRRs), and fatty acids play important roles [6, 7]. According to the hygiene hypothesis, exposure to innocuous microorganisms may lower the risk of allergic disease and supports gut-targeted approaches to lung disease, including probiotics [8–10]. Most probiotic research has focused on Lactobacillus and Bifidobacterium genera, but other microorganisms, including Saccharomyces yeasts, have also been investigated [11–14].

Probiotics act via multiple mechanisms, such as enhancement of the intestinal barrier, prevention of intestinal adhesion of enteropathogens, production of antimicrobial substances and of short-chain fatty acids (SCFAs), suppression of NLRP3, interaction of Toll-like and C-type lectin receptors, alteration of the intestinal microbiota, expansion of regulatory T lymphocytes, and modulation of the immune system [6, 7, 14, 15]. Oral treatment with live probiotics attenuated major features of asthma via a Toll-like receptor 9–dependent mechanism and was associated with increased regulatory T cells [13, 16, 17]. C-type lectin receptors (e.g., Mincle, Dectin-1) can directly interact with probiotics, modulating innate and adaptive immune responses [18]. Probiotic strains, especially from the genera Bifidobacterium and Lactobacillus, can directly produce SCFAs or promote the production of endogenous SCFA-producing bacteria [5, 19]. Probiotics may also alter medium- (e.g., caproic, caprylic, capric, and dodecanoic) and long-chain fatty acids (palmitic, stearic, oleic, linoleic, α-linolenic acid, dihomo-γ-linolenic, and arachidonic acid) [20, 21].

In addition, metabolic products of probiotics (known as postbiotic) may also exert beneficial effect [22, 23]. Previous studies have shown that postbiotics are safe, have anti-inflammatory effects, and can improve chronic diarrhea in young adults [24–26]. Conversely, their benefits have not yet been demonstrated for other diseases, such as allergy [24, 25]. Given that the effects of probiotics are strain- and disease-specific, it is crucial to evaluate their mechanisms of action within the context of each specific disease [27].

Saccharomyces cerevisiae UFMG A-905 was isolated from “cachaça”, a traditional Brazilian sugarcane-distilled alcoholic beverage. It has been shown to prevent bacterial infections, experimental colitis and mucositis, and food allergy [15, 28–30]. S. cerevisiae UFMG A-905 reduced inflammation and improved clinical signs in acute ulcerative colitis [15]. In mucositis models, it preserved mucosal barrier integrity and reduced oxidative stress [31, 32]. In a prior food-allergy study, S. cerevisiae UFMG A-905 significantly attenuated tissue inflammation and myeloperoxidase activity, and these effects were dependent on yeast viability [33]. In an animal model, S. cerevisiae UFMG A-905 prevented asthma development in a dose-dependent manner and, with perinatal administration, prevented asthma-like characteristics in the offspring [14, 33, 34]. Moreover, bread fermented with this strain with live S. cerevisiae UFMG A-905 in alginate microcapsules reduced allergic features of asthma in mice [35]. However, the underlying mechanisms remain unclear. In the present study, we describe the potential mechanisms by which S. cerevisiae UFMG A-905 prevents asthma, including the induction of regulatory T cells, activation of Th17 responses, and increased production of fatty acids.

Methods

Probiotic yeast and postbiotic

The yeast S. cerevisiae UFMG A-905 belongs to the culture collection of Prof. Dr. Carlos Augusto Rosa, Laboratory of Yeast Ecology and Biotechnology, Federal University of Minas Gerais (Belo Horizonte, MG, Brazil). The yeast was stored at − 80 °C in medium containing 20% glycerol, 2% peptone, and 1% yeast extract. For all experiments, it was cultured in yeast extract–peptone–dextrose (YPD; 1% yeast extract, 1% peptone, 2% dextrose) at 37 °C for 24 h. The culture was then concentrated by centrifugation to obtain 109 colony-forming units (CFU)/mL. To obtain material for experiments with postbiotic, culture aliquots were centrifuged at 5,000 rpm for 5 min and the supernatant collected and reserved to be administered to the mice.

Animals

Specific pathogen–free (SPF) male BALB/c mice (5–6 weeks old) were used to assess lung dendritic cells and regulatory T cells, pulmonary gene expression, fecal long-, medium-, and SCFAs, and intestinal cytokines. In complementary experiments, Il17a⁻/⁻ mice on a C57BL/6 background were used to determine the contribution of IL-17A to the yeast’s mechanism. Animals came from the breeding facility of the Ribeirão Preto Medical School (FMRP-USP), Ribeirão Preto, SP, Brazil, and maintained in individual autoclaved cages per the treatment protocol. Food and water were autoclaved weekly and supplied ad libitum. Euthanasia was performed by intraperitoneal overdose of a combination of ketamine (300 mg/kg) and xylazine (30 mg/kg) followed by exsanguination. The study was approved by the FMRP-USP Ethics Committee on Animal Use (protocol no. 022/2011).

Experimental asthma model and administration of probiotics and postbiotic

Mice received two intraperitoneal sensitizations, 7 days apart, each with 10 μg ovalbumin (OVA; Sigma grade V, Sigma-Aldrich) plus 1 mg aluminum hydroxide [Al(OH)₃]. After 1 week, they were challenged intranasally with 50 μL OVA (10 μg) under light anesthesia for three consecutive days. Yeast suspension was given via gavage daily, starting 10 days before the first sensitization and continuing throughout the sensitization and challenge protocol (total of 28 days). Mice received 100 μL per day of a suspension containing 109 CFU/mL of S. cerevisiae UFMG A-905. A separate group received 100 μL of the culture supernatant (postbiotic). Control groups received PBS on the same days (Supplementary information, Figure S1). Experimental design was identical for BALB/c mice and Il17a⁻/⁻ mice.

Yeast recovery

Bronchoalveolar lavage (BAL) samples were collected and cultured on Sabouraud dextrose agar (Difco, Sparks, NV, USA) supplemented with 100 mg/L of chloramphenicol and incubated at 37 °C during 48 h to detect the presence of the yeast.

Collection of bronchoalveolar lavage and cell counting

Bronchoalveolar lavage (BAL) was collected by instilling and subsequently withdrawing 1 mL of cold saline via the tracheal cannula, and total and differential cell counts (macrophages, eosinophils, neutrophils, and lymphocytes) were subsequently performed [14, 36]. Total cell counts were measured by trypan blue exclusion. Subsequently, BAL samples were centrifuged using a Cytospin (Cytospin IV, Thermo Scientific, Runcorn, Cheshire, CT, USA), stained with the Quick Panoptic kit (Laborclin, Pinhais, PR, Brazil), and differential counts were obtained by analyzing 300 inflammatory cells per slide.

Tissue preparation for flow cytometer

Following BAL collection, the mice were euthanized, and their lungs, spleen, and mesenteric lymph nodes were excised. Lung tissue was cut into small fragments and digested with a solution containing 0.5 µg/mL of liberase (Liberase Blendzyme, Roche, IN, USA), 25 U/mL of deoxyribonuclease I (Dnase, Sigma-Aldrich, MO, USA), and RPMI-1640 (Sigma-Aldrich). After, the tissue was incubated, centrifuged, and 10⁶ cells were obtained. Mesenteric lymph nodes were processed in RPMI medium supplemented with 10% fetal bovine serum, penicillin (Gibco, New York, NY, USA), and streptomycin (Gibco). The spleen was first fragmented and then processed in RPMI as described. After centrifugation, a cell suspension was obtained at a concentration of 10⁶ cells/mL.

Flow cytometer

Cell suspensions from the lungs, spleen, and mesenteric lymph nodes (1 × 106 cells) were incubated for 40 min at 4 °C with Fc Blocktm (BD Biosciences, Sao Jose, CA, USA) and for an additional 10 min at 4 °C with monoclonal antibodies. The following monoclonal antibodies were used: anti-CD11b (M1/70), anti-CD11c (HL3), anti-CD4 (H129.19), anti-CD25 (3C7), and anti-Foxp3 (FJK-16) from BD Biosciences (Sao Jose, CA, USA), and anti-MHCII (I-Ab/9/25/17), anti-CD103 (2E7) from Biolegend (San Diego, CA, USA). Antibody clones are listed in Table 1. Samples were acquired using a BD FACSCANTO II cytometer (BD Biosciences, Sao Jose, CA, USA). A total of 100,000 events per sample were collected and analyzed according to size, granularity, and fluorescence intensity using FlowJo software (Becton Dickinson and Company, Franklin Lakes, NJ, USA).

Table 1.

Antibodies used in flow cytometry assay

Population Antibodies Clone Manufacture
Lymphocytes CD4 (FITC) H129.19 BD Bioscience, USA
CD25(PE) 3C7 BD Bioscience, USA
FOXP3(APC) FJK-16 BD Bioscience, USA
Dendritic Cells CD11c APC HL3 BD Bioscience, USA
CD11b Pe Cy7 M1/70 BD Bioscience, USA
CD103 Pe 2E 7 BioLegend, USA
MHC Fitc M5/114.152 BioLegend, USA
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Cytokine analysis in the ileum and cecum

After thoroughly washing the ileum and cecum with cold PBS to remove luminal contents, the tissues were weighed and measured. Each sample was then homogenized in 1 mL of PBS containing a protease inhibitor cocktail (Complete Inhibitor, Roche Diagnostics, Laval, Canada). The resulting supernatant was collected and used for cytokine quantification. Levels of IL-10, IL-13, and IL-17A were quantified using the BD OptEIA™ set (BD Biosciences) according to the manufacturer's instructions.

Measurement of OVA-specific IgE levels

Serum was collected, and OVA-specific IgE levels were measured as previously described [14]. Briefly, plates were OVA-coated (overnight, 4 °C), washed (PBS/0.05% Tween-20), and blocked (PBS/10% FBS). Serum (1:1 with blocking buffer) was added, followed by biotinylated antibody (1:1000) and streptavidin-HRP (1:250). Color was developed with TMB, stopped with 16% H₂SO₄, and read at 450 nm; results were reported as optical density.

Fatty acids quantification

Short-, medium-, and long-chain fatty acids were measured in fecal samples using a gas chromatographic method (GC-2014, SHIMADZU, Columbia, MD, USA). Fatty acids were extracted in Milli-Q water, followed by direct injection into a flame ionization detector using a silica capillary column (6890N GC, Agilent, Folsom, CA, USA). Helium was used as the carrier gas at a flow rate of 1.0 mL/min. The procedures were adapted from Zhao, Nyman et al., and Lu, Fan et al. [37, 38]. The nomenclature of fatty acids analyzed is listed in Table S1 (Supplementary information).

Gene expression analysis by qPCR

Total RNA was extracted from the lung tissue using a commercial RNA extraction kit, and cDNA was synthesized using reverse transcriptase. Gene expression was quantified by qPCR using Power SYBR® Green PCR Master Mix (Applied Biosystems, Foster City, CA, USA). Real-time PCR was performed on the StepOnePlus Real Time PCR System (Applied Biosystems) as previously described [32]. Results were analyzed based on the cycle threshold (CT), and relative gene expression was calculated using the 2−ΔΔCT method, where ΔΔCT = ΔΔCt (sample)—ΔΔCt (control), and ΔCt = Ct (target gene) – Ct (HPRT, normalizer). Primers were used for the following genes: TLR-9, NLRP3, Mincle, Dectin-1, and HPRT. Primer sequences are listed in Table S2 (Supplementary information).

Statistical analysis

Categorical variables are reported as percentages, and continuous data are presented as box-and-whisker plots (median, IQR; Tukey whiskers). Between-group comparisons used one-way or two-way ANOVA, followed by Bonferroni or Tukey post hoc tests as appropriate. A two-sided p < 0.05 was considered statistically significant. GraphPad Prism 5 (GraphPad Software, Inc., San Diego, CA, USA) was used for data analysis.

Results

S. cerevisiae UFMG A-905 increased dendritic cells and regulatory T cells in lung tissue

First, we examined whether S. cerevisiae UFMG A-905 was associated with changes in dendritic cells and regulatory T cells. The number of CD11c⁺MHCII⁺CD11b⁺CD103⁻ DCs in lung tissue was significantly higher in OVA/PBS group compared to SAL/PBS group (p < 0.001). The administration of S. cerevisiae UFMG A-905 significantly increased the number of CD11c⁺MHCII⁺CD11b⁺CD103⁻ DCs in lung tissue compared to OVA/PBS group (p < 0.01; Fig. 1D). No significant difference was observed in the number of CD11c⁺MHCII⁺CD11b⁻CD103⁺ DCs in lung tissue among groups (p > 0.05; Fig. 1C). Additionally, the administration of S. cerevisiae UFMG A-905 significantly increased the percentage of regulatory T lymphocytes (CD4+CD25+FOXP3+) in the lungs compared to OVA/PBS group (p < 0.05; Fig. 1G). There were no significant differences in the percentage of regulatory T lymphocytes (CD4⁺CD25⁺FOXP3⁺) among groups in the mesenteric lymph nodes and spleen (Supplementary Information, Figure S2). The gating strategy with representative images for flow cytometry analysis is shown in Fig. 1 (panels A-B and E–F).

Fig. 1.

Fig. 1

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Saccharomyces cerevisiae UFMG A-905 administration increases the number of CD11c⁺MHCII⁺CD11b⁺CD103⁻ dendritic cells and the percentage of regulatory T cells in lung tissue. Dendritic and regulatory cells were analyzed by flow cytometer. (A-B) Gating strategy used to identify dendritic cells. (C-D) Quantitative analysis of dendritic cells. (E-F) Gating strategy used to identify regulatory T cells. (G) Quantitative analysis of regulatory T cells. Values are shown as box-and-whisker plots (n = 8). *p < 0.05; **p < 0.01; SAL/PBS: BALB/c mice sensitized and challenged with saline, received PBS; OVA/PBS: BALB/c mice sensitized and challenged with ovalbumin (OVA), received PBS; OVA/Sac: BALB/c mice sensitized and challenged with OVA, received S. cerevisiae UFMG A-905

S. cerevisiae UFMG A-905 increased NLRP3 expression in lung tissue

Next, we assessed the association between S. cerevisiae UFMG A-905 and the expression of key innate immune receptors: NLRP3 (inflammasome), TLR9 (TLR), and the C-type lectin receptors Dectin-1 and Mincle. The expression of TLR-9 and NLRP3 was significantly decreased in the OVA/PBS group compared to SAL/PBS group (p < 0.05). The administration of S. cerevisiae UFMG A-905 significantly increased NLRP3 expression compared to OVA/PBS group (p < 0.05). The expression of TLR-9, Dectin-1, and Mincle in lung tissue was not significantly altered by S. cerevisiae UFMG A-905 (Fig. 2).

Fig. 2.

Fig. 2

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Effect of Saccharomyces cerevisiae UFMG A-905 on TLR-9 (A), NLRP3 (B), Dectin-1 (C), and Mincle (D) expression in lung tissue. Gene expression was performed by real-time-PCR. Values are shown as box-and-whisker plots (n = 7) * p < 0.05; SAL/PBS: BALB/c mice sensitized and challenged with saline, received PBS; OVA/PBS: BALB/c mice sensitized and challenged with ovalbumin (OVA), received PBS; OVA/Sac: BALB/c mice sensitized and challenged with OVA, received S. cerevisiae UFMG A-905

Effect of S. cerevisiae UFMG A-905 on fecal fatty acid production

After assessing associations with dendritic cells (DCs), Tregs, and gene expression, we evaluated whether administration of S. cerevisiae UFMG A-905 alters short-, medium-, and long-chain fatty acids. The levels of fecal fatty acids are shown in Fig. 3. There were no significant differences in the percentages of SCFAs (acetate, propionate, and butyrate) among the groups (p > 0.05). In OVA/PBS group, the percentage of dodecanoic acid and dihomo-γ-linolenic acid was significantly reduced, while oleic acid was significantly increased compared to SAL/PBS group (p < 0.001). The administration of S. cerevisiae UFMG A-905 significantly increased the percentage of dihomo-γ-linolenic acid and significantly decreased the percentage of dodecanoic acid and oleic acid, compared to OVA/PBS group (p < 0.05). No significant differences were observed in the levels of arachidonic acid, stearic acid, and palmitic acid among the groups (p > 0.05).

Fig. 3.

Fig. 3

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Saccharomyces cerevisiae UFMG A-905 increased the fecal percentage of dihomo-γ-linolenic acid and decreased the percentage of dodecanoic acid and oleic acid. Fatty acids were measured in fecal samples using a gas chromatographic method. (A-C) Short-chain fatty acids. (D) Medium-chain fatty acid. (E-I) Long-chain fatty acids. Values are shown as box-and-whisker plots (n = 8). * p < 0.05; **p < 0.001; SAL/PBS: BALB/c mice sensitized and challenged with saline, received PBS; OVA/PBS: BALB/c mice sensitized and challenged with ovalbumin (OVA), received PBS; OVA/Sac: BALB/c mice sensitized and challenged with OVA, received S. cerevisiae UFMG A-905

The effects of S. cerevisiae UFMG A-905 were partially dependent on IL-17

Because S. cerevisiae UFMG A-905 raised IL-17A levels, we further tested dependency on IL-17A using Il17a⁻/⁻ mice. In wild-type mice, OVA challenge resulted in a significant increase in total cell counts, eosinophil and lymphocytes numbers compared to SAL/PBS group (p < 0.001; p < 0.0001; p < 0.05, respectively). In contrast, Il17a⁻/⁻ mice showed no significant differences in total cell counts, eosinophils, or lymphocytes compared to SAL/PBS group (p > 0.05). The administration of S. cerevisiae UFMG A-905 significantly reduced the number of eosinophils compared to the OVA challenge group in wild-type mice, but not in Il17a⁻/⁻ mice. No significant differences were observed in the numbers of macrophage, lymphocyte, and neutrophils in either wild-type or Il17a⁻/⁻ mice when compared to the OVA/PBS group (Fig. 4). Compared to OVA/PBS group, administration of S. cerevisiae UFMG A-905 led to a significant reduction in IL-13 levels in wild-type mice, but not in Il17a⁻/⁻ mice (Fig. 4).

Fig. 4.

Fig. 4

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Effects of Saccharomyces cerevisiae UFMG A-905 on airway total and differential cell counts and IL-13 levels in BALB/c wild-type and C57BL/6 Il17a⁻/⁻ mice. (A) Total cell counts. (B-E) Differential cell counts. (F) IL-13 levels. Values are shown as box-and-whisker plots (n = 8). *p < 0.05; **p < 0.01; ***p < 0.001; SAL/PBS: mice sensitized and challenged with saline, received PBS; OVA/PBS: mice sensitized and challenged with ovalbumin (OVA), received PBS; OVA/Sac: mice sensitized and challenged with OVA, received S. cerevisiae UFMG A-905

Serum levels of OVA-Specific IgE

OVA challenge resulted in a significant increase in OVA-specific IgE levels in both wild-type and Il17a⁻/⁻ mice compared to SAL/PBS group. Administration of S. cerevisiae UFMG A-905 did not significantly alter OVA-specific IgE levels in either group (Supplementary information, Figure S3).

Yeast recovery in the BAL and cytokine levels in the ileum and cecum

Next, considering the gut–lung axis, we evaluated whether S. cerevisiae UFMG A-905 altered cytokine levels in the gut and whether the yeast was present in the BAL. No yeast growth was detected in the BAL. The levels of IL-10, IL-13, and IL-17A in the ileum and cecum did not change significantly among groups (Supplementary information, Figure S4).

Postbiotic of S. cerevisiae UFMG A-905 supernatant did not change airway inflammation

Finally, to test whether the observed effects required live S. cerevisiae UFMG A-905 rather than yeast-derived products, we examined a postbiotic preparation. The numbers of total cells, eosinophils, and lymphocytes were significantly increased in the BAL of OVA/PBS group compared to SAL/PBS group (p < 0.01, p < 0.0001, and p < 0.05, respectively). The administration of S. cerevisiae UFMG A-905 supernatant did not significantly alter the numbers of total cells, eosinophils, macrophages, lymphocytes, and neutrophils in the BAL (Fig. 5; p > 0.05).

Fig. 5.

Fig. 5

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Postbiotic derived from Saccharomyces cerevisiae UFMG A-905 did not change the airway cellular response. (A) Total cell counts. (B-E) Differential cell counts. Values are shown as box-and-whisker plots (n = 8). * p < 0.05; **p < 0.01; ****p < 0.0001; SAL/PBS: BALB/c mice sensitized and challenged with saline, received PBS; OVA/PBS: BALB/c mice sensitized and challenged with ovalbumin (OVA), received PBS; OVA/Sac: BALB/c mice sensitized and challenged with OVA, received S. cerevisiae UFMG A-905

Discussion

S. cerevisiae UFMG A-905 attenuates asthma-like features, including bronchial hyperresponsiveness, airway and lung inflammation, and mucus production, in a dose-dependent manner, and also confers protection in offspring [14, 33, 34]. In this study, we demonstrate that S. cerevisiae UFMG A-905 exerts its effects through multiple mechanisms, including immune modulation, inflammasome activation, and enhanced anti-inflammatory fatty acid production.

The administration of S. cerevisiae UFMG A-905 increased regulatory T cells (CD4+CD25+FOXP3+) and dendritic cells (CD11c⁺MHCII⁺CD11b⁺CD103⁻) in the lungs. Regulatory T cells are a well-described hallmark response to several probiotics. Consistent with this, S. cerevisiae UFMG A-905 also enhanced the production of the anti-inflammatory cytokine IL-10 [30]. Since regulatory T cells are a major source of IL-10, this association may represent one mechanism of action. Although regulatory T cells increased in the lungs, no significant changes were detected in the mesenteric lymph nodes or spleen. Similarly, the levels of IL-10, IL-13, and IL-17 in the ileum and cecum remained unaltered. These findings suggest that the anti-inflammatory effect of S. cerevisiae UFMG A-905 was initiated in the gut but manifests locally in the lungs.

Regulatory T cells (Tregs) regulate both innate and adaptive immune responses. The major subpopulations relevant to asthma are natural (thymic; nTregs) and induced (peripheral; iTregs), which suppress type-2 and type-17 airway inflammation, promote tolerance and resolution, and limit airway hyperresponsiveness and remodeling. T follicular regulatory (Tfr) cells are another Treg subset that controls allergic responses. Additional populations include type 1 regulatory T cells (Th1‐like Tregs) involved in allergen tolerance and Th17-like Tregs implicated in Th17-driven inflammation [39, 40]. Further studies are needed to determine which Treg subpopulation(s) mediate the effects of S. cerevisiae UFMG A-905.

Dendritic cells (e.g., CD11c⁺CD11b⁺CD103⁻) have been associated with the stimulation of chemokines and cytokines, as well as the modulation of specific cell subsets. Under allergic inflammation, they contribute to the induction of Th2 and Treg response profiles [41]. A recent study characterized this cell population as CD11b⁺CD24⁺ and linked this phenotype to a Th17-type response upon challenge with Aspergillus fumigatus [41]. In our study, the administration of S. cerevisiae UFMG A-905 led to an increase in the phenotypic population of CD11c⁺MHCII⁺CD11b⁺CD103⁻ DC. The precise role of this DC phenotype in the lung remains unclear, and additional studies using an expanded panel (e.g., CD64, CD24, XCR1, Ly6C, Siglec-F) and functional assays (cytokine production; DC–T-cell co-culture) are needed to define and test this subset’s function. However, the increase of this population in the OVA/PBS group suggests that OVA stimulus, in conjunction with the pulmonary microenvironment, may have promoted DC activation and receptor engagement, leading to the induction of a Th2-type response. Interestingly, a further increase in this DC phenotype was observed following S. cerevisiae UFMG A-905 administration, which could reflect yeast-driven stimulation in the gut with downstream modulation via the gut–lung axis. We hypothesize that improvement in asthma characteristics may be mediated by the simultaneous induction of Treg and Th17 responses, leading to a decrease in the Th2 response [42].

While many studies link NLRP3 inflammasome upregulation to asthma severity [43], other reports diverge. A previous study evaluated four allergic asthma models (acute and chronic OVA and house dust mite) and observed only a modest and selected role for NLRP3 in one model, in the alum-free OVA model [44]. Another study reported that their model did not require NLRP3 activation or the interleukin-1 signaling axis [45]. In helminth infection models, classically type 2 immunity, the NLRP3 inflammasome exhibited differential roles during the innate and adaptive phases [46, 47]. Potential explanations include differences in antigen type and concentration, route and timing of administration, and host microbiome [43]. Of note, S. cerevisiae UFMG A-905 stimulated the expression of NLRP3, a cytoplasmic multiprotein complex activated by PAMPs and DAMPs. NLRP3 is involved in the cleavage of IL-1β, IL-18, and Caspase-1, triggering a pro-inflammatory response [48]. Gross et al. demonstrated that cells stimulated with Candida albicans and S. cerevisiae can induce NLRP3 expression via SYK signaling pathway [49]. Therefore, the presence of S. cerevisiae UFMG A-905 in the gut may have contributed to the activation of inflammasomes in our model.

Previous studies have demonstrated that the increased SCFAs production is one possible mechanism of action for probiotics. Schneider et al. demonstrated that Saccharomyces boulardii administration in patients receiving enteral nutrition presented increased levels of butyrate and total fatty acids in the feces [50]. In our study, oral administration of S. cerevisiae UFMG A-905 did not increase SCFAs levels in the feces. However, we cannot rule out the possibility that the levels were increased in the serum, but not detectable in the feces. Interestingly, S. cerevisiae UFMG A-905 increased the levels of the long-chain fatty acid dihomo-γ-linolenic acid, which serves as a substrate for cyclooxygenase (COX) enzymes and a precursor of prostaglandin E1, a molecule known for its anti-inflammatory effects [51, 52]. Consistent with our results, reduced dihomo-γ-linolenic acid levels have been observed in a house dust mite model of asthma [53]. Dihomo-γ-linolenic acid has been reported to be inversely associated with lung function and bronchial hyperresponsiveness [54, 55]. Potential mechanisms include changes in prostaglandin E1 production, relaxation of bronchial smooth muscle, and modulation of arachidonic acid–derived cysteinyl leukotrienes [52, 54, 56]. To establish a causal role for the potential beneficial effect of dihomo-γ-linolenic acid, further studies using exogenous administration are needed to determine whether it can mimic the yeast’s protective effects.

Subsequently, we used Il17a⁻/⁻ mice to evaluate its role in the mechanism of action of S. cerevisiae UFMG A-905. In wild-type C57BL/6 mice, administration of S. cerevisiae UFMG A-905 significantly reduced eosinophil counts and IL-13 levels. In contrast, in Il17a⁻/⁻ mice, S. cerevisiae UFMG A-905 did not reduce eosinophil numbers or IL-13 levels, suggesting that its effects are partially dependent on IL-17A. These findings support our hypothesis that the Th17 response stimulated by S. cerevisiae UFMG A-905 contributes to the reduction of key features of asthma. Finally, postbiotic administration did not alter airway inflammation, reinforcing the necessity of live yeast, rather than its metabolic products alone, to reduce airway cellular responses [57]. However, as the postbiotic was not evaluated in further experiments, we cannot rule out effects on other aspects of allergic responses.

Limitations of this study

This study has several limitations. First, most experiments used BALB/c mice, and to investigate the role of IL-17A, we used a C57BL/6 background, which introduces potential strain-specific immune differences. However, we do not directly compare BALB/c with C57BL/6, and the IL-17A effects are inferred within the C57BL/6 background. In addition, we did not evaluate other knockout models, nor did we measure SCFAs in mouse serum. Moreover, cytokine quantification and gene expression were performed only in one time point; ideally, measurements would have been conducted at multiple time points, prior to sensitization, during, and following the administration of S. cerevisiae UFMG A-905. Third, because gene expression was measured in whole-lung tissue, we cannot comprehensively determine which pathways are up- or down-regulated. Further experiments focusing on defined cell populations or signaling pathways are needed. Fourth, although dihomo-γ-linolenic acid has emerged as a potential anti-inflammatory fatty acid, we did not investigate its isolated effect either in vivo or in vitro studies. Fifth, we measured only NLRP3 gene expression, and assessment of upstream or downstream markers would also be important to corroborate inflammasome activation. Another important limitation is the inherent challenge of translating findings from animal models to human asthma, as differences in immune responses and disease complexity may limit direct clinical applicability. Additionally, although we previously showed that S. cerevisiae UFMG A-905 prevented asthma-like characteristics in both male and female offspring [34], the current experiments were conducted exclusively in male mice, which could introduce a sex bias. Finally, under the 3Rs principles, we did not include a saline-sensitized control group receiving S. cerevisiae UFMG A-905. However, preliminary results (data not shown) indicated no significant effect of the yeast in this control group.

Conclusion

The effects of S. cerevisiae UFMG A-905 in a murine asthma model correlated with multiple mechanisms. These include the stimulation of Th17, dendritic-cell and regulatory T-cell responses, upregulation of NLRP3 expression, and increased production of dihomo-γ-linolenic acid. Additionally, the absence of detectable local effects in the gut suggests the involvement of the gut–lung axis in these outcomes.

Supplementary Information

Supplementary Material 1. (320KB, docx)

Acknowledgements

This study was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior—Brasil (CAPES)—Finance Code 001 and by the National Council for Scientific and Technological Development (CNPq), Brazil. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Authors’ contributions

Conceptualization: Vanessa M. B. Fonseca, Alceu A. Jordão Junior, Jacques R. Nicoli, Flaviano S. Martins, and Marcos C. Borges; Methodology: Vanessa M. B. Fonseca, Camila M. Sandy, Camila C. Guimarães, Alceu A. Jordão Junior, and Marcos C. Borges; Data collection and analysis: Vanessa M. B. da Fonseca, Camila M. Sandy, Camila C. Guimarães, Alceu A. Jordão Junior, Jacques R. Nicoli, Flaviano S. Martins, and Marcos C. Borges; Writing original draft preparation: Vanessa M. B. Fonseca and Marcos C. Borges; Writing review and editing: Vanessa M. B. Fonseca, Camila M. Sandy, Camila C. Guimarães, Alceu A. Jordão Junior, Jacques R. Nicoli, Flaviano S. Martins, and Marcos C. Borges. All authors read and approved the final manuscript.

Data availability

The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

The study was approved by the Ethics Committee on Animal Use of the Ribeirão Preto Medical School, University of São Paulo (FMRP-USP) (protocol no. 022/2011).

Consent to publication

Not applicable.

Competing interests

The authors declare no competing interests.

Footnotes

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Associated Data

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Supplementary Materials

Supplementary Material 1. (320KB, docx)

Data Availability Statement

The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.

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