Abstract
This study was conducted to determine if oral administration of the novel herbal medicine, MA, and its Lactobacillus acidophilus fermented product, MA128, have therapeutic properties for the treatment of asthma. Asthma was induced in BALB/c mice by systemic sensitization to ovalbumin (OVA) followed by intratracheal, intraperitoneal, and aerosol allergen challenges. MA and MA128 were orally administered 6 times a week for 4 weeks. At 1 day after the last ovalbumin exposure, airway hyperresponsiveness was assessed and samples of bronchoalveolar lavage fluid, lung cells, and serum were collected for further analysis. We investigated the effect of MA and MA128 on airway hyperresponsiveness, pulmonary eosinophilic infiltration, various immune cell phenotypes, Th2 cytokine production, OVA-specific IgE production, and Th1/Th2 cytokine production in this mouse model of asthma. In BALB/c mice, we found that MA and MA128 treatment suppressed eosinophil infiltration into airways and blood, allergic airway inflammation and AHR by suppressing the production of IL-5, IL-13, IL-17, Eotaxin, and OVA-specific IgE, by upregulating the production of OVA-specific Th1 cytokine (IFN-γ), and by downregulating OVA-specific Th2 cytokine (IL-4) in the culture supernatant of spleen cells. The effectiveness of MA was increased by fermentation with Lactobacillus acidophilus.
Highlights
Asthma is a chronic, complex respiratory disease caused by various airway obstructions, airway eosinophilic inflammation, and bronchial hyperresponsiveness [1]
IL-4 can directly induce airway hyperresponsiveness and airway and blood eosinophilia in asthmatic patients [4], and other investigators have shown an inhibitory effect of IFN-γ on pulmonary allergic responses [5]
Th2 cytokines produced by CD4+ T cells, such as interleukin-4 (IL-4), IL-5, and IL-13, enhance immunoglobulin E (IgE) production and eosinophil accumulation, and IL-13 directly enhances mucus hypersecretion and Airway Hyperresponsiveness (AHR) [7, 8]
Summary
Complex respiratory disease caused by various airway obstructions, airway eosinophilic inflammation, and bronchial hyperresponsiveness [1]. IL-4 can directly induce airway hyperresponsiveness and airway and blood eosinophilia in asthmatic patients [4], and other investigators have shown an inhibitory effect of IFN-γ on pulmonary allergic responses [5]. CD4+ T cells play a crucial role in immune protection through their capacity to help B cells make antibodies, to recruit neutrophils, eosinophils, and basophils to sites of inflammation, and, through their production of cytokines and chemokines, to orchestrate immune responses [6]. Suppression of cytokine production in activated CD4+ T cells may be useful for the treatment of asthma. Suppression of Th2 cytokine production in activated CD4+ Th cells may be useful for the treatment of inflammatory immune diseases including asthma
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
