Abstract
We aimed to explore the imbalance between the T helper 17 γδT cells (γδT17) and the regulatory γδT cells (γδTreg) in asthmatic mice. Male Balb/c mice were randomly divided into the normal control group and the asthmatic model group. The asthmatic model group mice were intraperitoneally injected with the mixture of ovalbumin (OVA)/Al(OH)3 and then activated by exposure of the animals to OVA atomization. Airway hyperresponsiveness (AHR) was determined by a non-invasive lung function machine. Hematoxylin and eosin and Alcian blue-periodic acid Schiff staining were done for histopathological analysis. Interleukin (IL)-17 and IL-35 levels in bronchoalveolar lavage fluid were detected by ELISA. The percentage of IL-17+ γδT cells and Foxp3+ γδT cells in spleen cells suspension were detected and the transcription levels of RORγt and Foxp3 in the lung tissue were determined. Compared with the normal control, the severity of airway inflammation and AHR were higher in the asthmatic mice. Furthermore, mice in the asthmatic group displayed significant increases of IL-17+ γδT cells, expression of IL-17A, and RORγt, whereas control mice displayed marked decreases of Foxp3+ γδT cells, expression of IL-35, and transcription factor Foxp3. In addition, the mRNA expression of RORγt was positively correlated with the percentage of IL-17+γδT cells, and the mRNA level of Foxp3 was positively correlated with the percentage of Foxp3+ γδT cells. The imbalance of γδT17/γδTreg in the asthmatic mice may contribute to the pathogenesis of OVA-induced asthma.
Highlights
Bronchial asthma is a chronic inflammatory airway disease characterized by airway inflammation, airway hyper-responsiveness (AHR) and airway wall remodeling [1]
Studies have shown the potential role of gd regulatory T cells in inhibiting antitumor immune responses in patients diagnosed with multiple myeloma [12]
The aim of this study was to explore the imbalance of gdT17/gdTreg cells and related changes in cytokine expression in the pathogenesis of asthmatic mice and to further elucidate whether this imbalance is associated with alternation of inflammation in OVA-induced asthma
Summary
Bronchial asthma is a chronic inflammatory airway disease characterized by airway inflammation, airway hyper-responsiveness (AHR) and airway wall remodeling [1]. Emerging evidence has suggested that gdT cells, a T cell subset, have a critical role in the pathogenesis of asthma, such as airway inflammation and remodeling through the release of cytokines [4,5]. It has previously been reported that gdT17 cells, as important proinflammatory cells that produced the IL-17 cytokine, were associated with the pathogenesis of various inflammation diseases, such as bronchial asthma, cancer, skin inflammation, and others [8,9,10]. Studies have shown the potential role of gd regulatory T cells in inhibiting antitumor immune responses in patients diagnosed with multiple myeloma [12]. Studies on the relation of gdT17 cells and gdTreg cells in ovalbumin (OVA)-induced asthma are poorly reported
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