ArticleMolecular medicine reports2020
Effect of IL‑7 on Th17 cell responses in a mouse model of neutrophilic asthma.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Neutrophilic asthma: advances in experimental models from pathogenesis to therapeutic translation.Molecular medicine (Cambridge, Mass.) · 2026Review
- Distinct single-cell transcriptional profile in CD4+ T-lymphocytes among obese children with asthma.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Serological markers, pulmonary function, and prognosis in pediatric asthma: predictive model development and validation.American journal of translational research · 2025Article
- Tiotropium Bromide Has a More Potent Effect Than Corticosteroid in the Acute Neutrophilic Asthma Mouse Model.Tuberculosis and respiratory diseases · 2022Article
- AKR1C1 alleviates LPS‑induced ALI in mice by activating the JAK2/STAT3 signaling pathway.Molecular medicine reports · 2021Article
- miR‑29a‑3p regulates the epithelial‑mesenchymal transition via the SPARC/ERK signaling pathway in human bronchial epithelial cells.International journal of molecular medicine · 2021Article
- Relationship between Th17-mediated immunity and airway inflammation in childhood neutrophilic asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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