Lactococcus lactis NZ9000 Prevents Asthmatic Airway Inflammation and Remodelling in Rats through the Improvement of Intestinal Barrier Function and Systemic TGF-β Production

Abstract

<b><i>Introduction:</i></b> The use of probiotics has been broadly popularized due to positive effects in the attenuation of aberrant immune responses such as asthma. Allergic asthma is a chronic respiratory disease characterized by airway inflammation and remodelling. <b><i>Objective:</i></b> This study was aimed to evaluate the effect of oral administration of <i>Lactococcus lactis</i> NZ9000 on asthmatic airway inflammation and lung tissue remodelling in rats and its relation to the maintenance of an adequate intestinal barrier. <b><i>Methods:</i></b> Wistar rats were ovalbumin (OVA) sensitized and challenged and orally treated with <i>L. lactis</i>. Lung inflammatory infiltrates and cytokines were measured, and remodelling was evaluated. Serum OVA-specific immunoglobulin (Ig) E levels were assessed. We also evaluated changes on intestinal environment and on systemic immune response. <b><i>Results:</i></b> <i>L. lactis</i> diminished the infiltration of proinflammatory leucocytes, mainly eosinophils, in the bronchoalveolar compartment, decreased lung IL-4 and IL-5 expression, and reduced the level of serum allergen-specific IgE. Furthermore, <i>L. lactis</i> prevented eosinophil influx, collagen deposition, and goblet cell hyperplasia in lung tissue. In the intestine, <i>L. lactis</i>-treated asthmatic rats increased Peyer’s patch and goblet cell quantity and mRNA expression of IgA, MUC-2, and claudin. Additionally, intestinal morphological alterations were normalized by <i>L. lactis</i> administration. Splenocyte proliferative response to OVA was abolished, and serum levels of transforming growth factor (TGF)-β were increased by <i>L. lactis</i> treatment. <b><i>Conclusions:</i></b> These findings suggest that <i>L. lactis</i> is a potential candidate for asthma prevention, and the effect is mediated by the improvement of intestinal barrier function and systemic TGF-β production.