Abstract
Shuang-Huang-Lian (SHL), an herbal formula of traditional Chinese medicine, is clinically used for bronchial asthma treatment. Our previous study found that SHL prevented basophil activation to suppress Th2 immunity and stabilized mast cells through activating its mitochondrial calcium uniporter. Sporadic clinical reports that SHL was used for the treatment of bronchial asthma can be found. Thus, in this study, we systematically investigated the effects of SHL on asthmatic responses using a shrimp protein (SP)- induced mouse model. SHL significantly inhibited airway inspiratory and expiratory resistance, and histological studies suggested it reduced thickness of airway smooth muscle and infiltration of inflammation cells. It also could alleviate eosinophilic airway inflammation (EAI), including reducing the number of eosinophils and decreasing eotaxin and eosinophil peroxidase levels in the bronchoalveolar lavage fluid (BALF). Further studies indicated that SHL suppressed SP-elevated mouse mast cell protease-1 and IgE levels, prevented Th2 differentiation in mediastinal lymph nodes, and lowered Th2 cytokine (e.g., IL-4, IL-5, and IL-13) production in BALF. In conclusion, SHL attenuates airway hyperresponsiveness and EAI mainly via the inhibition of mast cell activation and Th2 immunity, which may help to elucidate the underlying mechanism of SHL on asthma treatment and support its clinical use.
Highlights
Asthma is a chronic inflammatory disease of the airways
We investigated the protective effects of SHL on asthmatic responses using a shrimp protein (SP)- induced murine asthma model
airway hyperresponsiveness (AHR) was tested by measuring airway resistance in response to Mch ranging from 0.025 mg/kg to 0.2 mg/kg 24 h after the last nebulization of SP
Summary
Asthma is a chronic inflammatory disease of the airways. Asthma is divided into allergic and nonallergic forms, which are distinguished by the presence or absence of clinical allergic reaction and in vitro IgE response to specific aeroallergens [2]. Characteristic to both forms is the airway wall accumulation of activated Th2 cells, whose cytokines can drive infiltration of eosinophils [3]. IL-4 promotes IgE production by B cells [4], IL-5 causes development, recruitment, and activation of eosinophils [5], and IL-13 controls the effector phase of asthma by inducing airway hyperresponsiveness (AHR) and airway remodeling (AR), as well as hyperproduction of mucus [6]
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