Abstract
Aeroallergens such us the spores of Alternaria alternata are described as the most important agents associated with respiratory allergies and severe asthma. Various experimental models of asthma have been developed using A. alternata extracts to study the pathogenesis of asthma, establishing the main parameters that trigger the asthmatic response. In this study, we describe a mouse model of asthma induced only by Alt a 1. To induce the allergic response, mice were challenged intranasally with the major allergen of A. alternata, Alt a 1. The presence of eosinophils in the lungs, elevated concentrations of Th2 family cytokines, lymphocyte proliferation and elevated IgE total serum levels indicated that the sensitisation and challenge with Alt a 1 induced the development of airway inflammation. Histological studies showed an eosinophilic cellular infiltrate in the lung tissue of mice instilled with Alt a 1. We demonstrate that Alt a 1 alone is capable of inducing a lung inflammatory response with an increase in IgE serum levels mimicking the allergic asthma immunoresponse when it is administered into BALB/c mice. This model will allow the evaluation of the immunoregulatory or immunotolerant capacity of several molecules that can be used in targeted immunotherapy for fungal allergic asthma.
Highlights
Native Alt a 1 was obtained from A. alternata extracts produced in our laboratory, while recombinant Alt a 1 was produced in E. coli C43 (DE3) pLyss strain (Lucigen)
In both the extract and nAlta 1, a dimeric protein of 14.5 kDa molecular weight was observed and, a 25 kDa molecular weight protein was detected in rAlt a 1
We established a murine model of allergic asthma that reproduced the fundamental parameters of asthmatic disease, using the major allergen of A. alternata, and fundamental parameters of asthmatic disease, using the major allergen of A. alternata, and
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Asthma is a complex inflammatory disease clinically characterised by airway hyperresponsiveness, inflammatory cell infiltration in the bronchoalveolar lavage (BAL). Bronchial walls and structural changes to the airway [1]. Asthma affects more than 300 million people worldwide [2] and type 2 allergic asthma is one of the most widespread phenotypes of the disease [3]. The entry and recognition of allergens by the antigenpresenting cells (APC) triggers a series of immune responses in which Th2 cells and innate lymphoid cells type 2 (ILC2) play a major role in the development of inflammation and allergic response [4]. Th2 cells participate in the adaptive immune response, producing
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