Effect of IL‑7 on Th17 cell responses in a mouse model of neutrophilic asthma
- Xiaobo Zhang
- Min Zhang
- Min Jiang
- Guangmin Nong
Affiliations: Pediatric Department, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China, Pediatric Department, People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China
- Published online on: May 27, 2020 https://doi.org/10.3892/mmr.2020.11191
Copyright: © Zhang
et al. This is an open access article distributed under the
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Neutrophilic asthma (NA) is characterized by neutrophil‑mediated inflammation and the presence of Th17 cells. However, the mechanisms underlying Th17 cell responses in NA remain unknown. The aim of the present study was to examine the effects of interleukin (IL)‑7 on Th17 cell responses in NA. A NA mouse model was sensitized by airway delivery of ovalbumin (OVA) and lipopolysaccharide and challenged with 1% OVA aerosol from day 21 for 3 consecutive days. Airway resistance was then measured to assess airway hyper‑responsiveness (AHR). Cells from bronchoalveolar lavage fluid (BALF) underwent Diff‑Quick and hematoxylin and eosin staining for classification. The levels of IL‑17 in the BALF were determined by ELISA. The effects of IL‑7 administration and STAT5 inhibition on Th17 cells were also characterized in vitro using splenic CD4+ T cells. Ki‑67, Bcl‑2 and activated caspase‑3 expression in differentiated Th17 cells were analyzed by flow cytometry. The mouse model of NA was characterized by increased AHR, elevated levels of IL‑17, high neutrophil counts in BALF, accumulated inflammatory cells in the lung and Th17 cell responses. IL‑7 promoted the expression of Ki‑67 and Bcl‑2 while reducing caspase‑3 expression. STAT5 inhibitor treatment decreased the levels of Ki‑67 and Bcl‑2, and resulted in increased expression of caspase‑3. These results suggested that the IL‑7/JAK/STAT5 signaling pathway may be involved in Th17 cell responses in NA.