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Intranasal administration of OM-85, a bacterial lysate, alters lung transcriptional profiles and protects against experimental asthma

ABSTRACT: Background: Microbial interventions against allergic asthma have robust epidemiologic underpinnings and the potential to recalibrate disease-inducing immune responses. Oral administration of OM-85, a standardized lysate of human airways bacteria, is widely used empirically to prevent respiratory infections, and a clinical trial is testing its ability to prevent asthma in at-risk children. On the other hand, we previously showed that intra-nasal administration of products from microbe-rich farm environments abrogate experimental allergic asthma. Objectives: To investigate whether direct administration of OM-85 to the airway compartment protects against experimental allergic asthma, and to identify protective cellular and molecular mechanisms activated through this natural route. Methods: BALB/cJ mice (7-8 weeks old) sensitized and challenged with Ovalbumin received OM-85 intra-nasally, and cardinal cellular and molecular asthma phenotypes were measured. Murine lung gene expression was profiled by RNA-sequencing. Results: Airway administration of OM-85 suppressed allergic asthma and altered the transcriptome profile in unfractionated lung tissue. Conclusion We provide the first demonstration that administration of a standardized bacterial lysate to the airway compartment protects from experimental allergic asthma by engaging multiple immune pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE167867 | GEO | 2021/10/19

REPOSITORIES: GEO

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Intranasal administration of OM-85, a bacterial lysate, alters lung transcriptional profiles and protects against experimental asthma

Project description:Intranasal administration of OM-85, a bacterial lysate, alters lung transcriptional profiles and protects against experimental asthma

| PRJNA705359 | ENA

Gene exprssion at single cell level in patients broncoalveolar lavage (BAL) cells stimulated ex vivo with bacterial lysate OM-85

Project description:OM-85 is a bacterial lysate used in clinical practice to reduce duration and frequency of recurrent respiratory tract infections. Whereas knowledge on its regulatory effects in vivo has substantially advanced, the mechanisms of OM-85 sensing remain inadequately addressed.The purpose of this study was to investigate the transptomic profile of human airway immune cells in the BAL after ex vivo stimulation with OM-85 at the single cell level and determine to what extent OM-85-induced gene signature in different myeloid cell subsets is dependent on TLR2/TLR4 expression.

2024-03-16 | GSE261353 | GEO

Gene expression profile of human mono-derived DCs stimulated with the bacterial lysate OM-85

Project description:OM-85 is a bacterial lysate used in clinical practice to reduce duration and frequency of recurrent respiratory tract infections. Whereas knowledge on its regulatory effects in vivo has substantially advanced, the mechanisms of OM-85 sensing remain inadequately addressed.The purpose of this study was to investigate the transptomic profile of human mo-DCs after ex vivo stimulation with OM-85 at determine to what extent OM-85-induced gene signature in different myeloid cell subsets is dependent on TLR2/TLR4 expression. We also aimed to compare the OM-85-triggered gene signature with the signatures induced by specific TLR2 or TLR4 agonists.

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Targeting mitochondrial reactive oxygen species alleviates allergic airway disease in a mouse model of obese allergic asthma

Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.

2023-06-02 | PXD029715 | Pride

IL-22 inhibits allergic airway inflammation in house dust mite-induced asthma models

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Expression data from airway epithelial cells stimulated with Poly(I:C) from patients with asthma, rhinitis, and healthy controls

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2013-10-18 | E-GEOD-51392 | biostudies-arrayexpress

Transplacental Innate Immune Training via Maternal Microbial Exposure: Role of XBP1-ERN1 Axis in Dendritic Cell Precursor Programming

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2020-11-22 | GSE140143 | GEO

Pooled genome-wide analysis to identify novel risk loci for pediatric allergic asthma

Project description:We performed a pooled GWAS and individual genotyping in 269 children with allergic respiratory diseases comparing allergic children with and without asthma. We used a modular approach to identify the most significant loci associated with asthma by combining silhouette statistics and physical distance method with cluster-adapted thresholding. We found 97% concordance between pooled GWAS and individual genotyping, with 36 out of 37 top-scoring SNPs significant at individual genotyping level. The most significant SNP is located inside the coding sequence of C5, an already identified asthma susceptibility gene, while the other loci regulate functions that are relevant to bronchial physiopathology, as immune- or inflammation-mediated mechanisms and airway smooth muscle contraction. Integration with gene expression data (from mouse experimental asthma model taken from GSE6858 and GSE1301) showed that almost half of the putative susceptibility genes are differentially expressed in experimental asthma mouse models.

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Expression data from airway epithelial cells stimulated with Poly(I:C) from patients with asthma, rhinitis, and healthy controls

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A regulatory CD9+ B cell subset controls HDM-induced allergic airway inflammation

Project description:Background: A specific subset of regulatory IL-10 producing B cells has been extensively studied in autoimmune and inflammatory pathologies. These cells are able to constrain exacerbated inflammation by inhibiting T cell mediated responses and maturation of antigen presenting cells. In allergic diseases, observations that increase of regulatory B cells is necessary for allergen tolerance suggest that development of allergic asthma would be associated with a defect in the regulatory B cells compartment. Objective: We sought to (i) characterize regulatory IL-10+ regulatory B cell subset in Balb/c mice by microarray and flow cytometry and (ii) investigate their regulatory capacity in vivo in a house dust mite model of allergic asthma. Results: We identified an IL-10 producing B cells subset able to control T cell proliferation in vitro in both control and asthmatic mice. This subset is decreased in allergic mice. IL-10+ Breg cells express high levels of CD9 and upregulate CD70 and CD73 after activation. Expression of CD9 allows identifying more than 50% of Bregs. Interestingly CD9+ B cells inhibit TH2-TH17 allergic airway inflammation in vivo after adoptive transfer in an IL-10 dependent manner. Conclusions: Herein, we demonstrate that induction of allergic asthma dampens the generation of Bregs contributing to exacerbated airway inflammation. We identified a distinct CD9+ Breg-cell population decreased in lung of HDM mice and able to control asthma and allergic airway inflammation by producing IL-10 after adoptive transfer. This study points B cells as an interesting therapeutic target in allergic asthma. IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) in control mice + IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) from asthmatic allergic (HDM) mice

2015-03-01 | E-GEOD-57772 | biostudies-arrayexpress

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