Abstract
Allergic asthma is associated with T helper (Th) 2 cell-biased immune responses and characterized by the airway hyperresponsiveness (AHR). Studies have shown that the acupoint catgut-embedding therapy (ACE) has a therapeutic effect on allergic asthma. However, the relevant mechanism is poorly understood. In present study, female BALB/c mice were sensitized and challenged with ovalbumin (OVA) to establish a model of allergic asthma. AHR was evaluated by using airway resistance (RL) and lung dynamic compliance (Cdyn). Airway inflammation and mucus hypersecretion were observed by HE and PAS staining. Inflammatory cells were counted, and related cytokines in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Pulmonary group 2 innate lymphoid cell (ILC2s) proportions were analyzed by flow cytometry. The expression of nuclear factor κB (NF-κB) and cyclooxygenase-2 (COX-2) was detected by immunostaining. Our results showed that OVA induction resulted in a significant increase in RL, accompanied by a significant decrease in Cdyn. The levels of interleukin- (IL-) 4, IL-13, OVA-specific IgE in BALF, and the percentage of ILC2 in the lungs were markedly increased accompanied by a significant decreased in interferon-γ (IFN-γ). Furthermore, the expressions of p-NF-κB p65 and COX-2 in airways were significantly upregulated. After ACE treatment, the indicators above were significantly reversed. In conclusion, ACE treatment inhibited the secretion of Th2 cytokines and the proliferation of ILC2s in the lungs, thereby dampening the inflammatory activity in allergic asthma. The underlying mechanism might be related to the inhibition of NF-κB/COX-2 pathway.
Highlights
Allergic asthma is a complex immunologic and chronic inflammatory disease with a series of symptoms such as wheezing, shortness of breath, chest tightness, and coughing [1], which is closely associated with airway inflammation and airway remodeling, and characterized by the airway hyperresponsiveness (AHR)
Studies have shown that IL-4 can modify the activation of nuclear factor κB (NF-κB) induced by other agents [10], and NF-κB plays an important role in the pathogenesis of IL-13-induced tissue damage in asthma [11, 12]
Allergic asthma is characterized by AHR, which is evidenced by airway resistanceincrease (RL) and lung dynamic compliancedecrease (Cdyn) [23]
Summary
Allergic asthma is a complex immunologic and chronic inflammatory disease with a series of symptoms such as wheezing, shortness of breath, chest tightness, and coughing [1], which is closely associated with airway inflammation and airway remodeling, and characterized by the airway hyperresponsiveness (AHR). Cytokines secreted by Th2 cells such as IL-4 and IL-13 promote the proliferation and expansion of the ILC2s population in the lungs [9] Both Th2 cytokines and ILC2s are responsible for the asthmatic airway inflammation and may interact with each other to enhance the proinflammatory effects. As a downstream of NF-κB, COX-2 has been confirmed to be related to asthma airway inflammation, it can be highly induced by a variety of stimulus such as cytokines [14] and oxidative stress [15], and its expression has been shown to be significantly elevated in both asthmatic patients and mice compared with normals [16, 17]. Studies have shown that COX-2 induced by NF-κB is an important mediator in the lung inflammation, and the expression of COX-2 can be enhanced by the activation of NF-κB. COX-2 itself participates in the activation process of NF-κB, leading to an induction of other inflammatory mediators and cells [18]
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