Allergic Asthma's pathomechanism is essentially a disruption of bronchial homeostasis characterized by an increase in proinflammatory mediators such as T and B effector cells, over immune regulatory cell signaling. Recent work has brought to the forefront the pivotal role of gut microbial metabolites, SCFAs, in abrogating the cardinal features of asthma, such as airway inflammation and AHR, via induction of tolerogenic pathways, tipping the balance towards homeostasis recovery.

The goal was to investigate on a broader scale the immune-regulatory role of propionate in allergic airway- inflammation, in vivo, in an asthma mouse model, and in vitro on human B cell behavior.

The preventive effect of propionate was tested in vivo by treating (or not) BALB/c mice with airway-delivered propionate during house dust mite (HDM) allergen induction of asthma, at the indicated time points. Asthma-related features such as airway function and inflammation were assessed through airway hyperresponsiveness (AHR) measurement, and immune cell profile analysis performed on blood, bronchoalveolar lavage fluid, lungs and spleen, respectively. In vitro, proliferation, survival and intracellular IL-10 expression of isolated purified human B cells was determined upon propionate treatment or not, by flow cytometry.

In vivo, Propionate treatment ameliorated AHR after allergic challenge and reduced eosinophil, neutrophil and T lymphocyte but not macrophages extraversion to the lungs. Lung tissue from propionate treated allergic mice showed increased Treg cells, decreased Th2 and Th17 cells and increased B regulatory IL-10 producing cells and Granzyme B cells compared to asthmatic controls. In vitro, propionate dose dependently reversed CPG, CD₄₀L induced B cell proliferation and IL-10 secretion.

Direct lung delivery of propionate improved allergen-induced airway inflammation by attenuating lung eosinophilia, neutrophilia and AHR. As well as Treg and B reg over effector cell differentiation in vivo and inhibited B cell Proliferation in vitro. Authors do not have conflict of interest to declare.