ArticleExperimental and therapeutic medicine2015
Interleukin-17A promotes the formation of inflammation in the lung tissues of rats with pulmonary fibrosis.
Article in Experimental and therapeutic medicine, 2015. 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, 10 citations in OpenAlex.
- Impact of Curcumin on the IL-17A-Mediated p53-Fibrinolytic System: Mouse Proteomics and Integrated Human Fibrosis scRNAseq Insights.Inflammation · 2025Article
- The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Article
- Bioinformatics Analysis Identifies Potential Ferroptosis Key Genes in the Pathogenesis of Pulmonary Fibrosis.Frontiers in genetics · 2021Article
- Clinical Role of Serum Interleukin-17A in the Prediction of RefractoryInfection and drug resistance · 2020Article
- Frequency of Th17 cells correlates with the presence of lung lesions in pigs chronically infected with Actinobacillus pleuropneumoniae.Veterinary research · 2017Article
- The Role of Cytokines in the Fibrotic Responses in Crohn's Disease.Frontiers in medicine · 2017Review
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the effects of interleukin (IL)-17A in a rat model of pulmonary fibrosis. In total, 20 female Wistar rats were randomly divided into a normal saline (NS group) and a bleomycin group (BLM group). The BLM group rats were intratracheally instilled with BLM, while the NS group rats were intratracheally instilled with saline. In each group, half the rats were sacrificed at day 7 and day 28, respectively, following intratracheal instillation. Subsequently, hematoxylin and eosin and Masson's trichrome staining were performed to observe the pathological changes in the lung tissue, while the expression of IL-17A in the lung tissue was detected by immunohistochemistry. In addition, the bronchoalveolar lavage fluid (BALF) was collected and divided into two sections. One section was used for cell counting and classification, and an ELISA was performed to detect the concentration of IL-17A in the BALF. The additional section was used to separate, purify and cultivate alveolar macrophages (AMs). The concentration of IL-17A in the cultivating supernatant was detected by ELISA, and the mRNA expression levels of IL-17A in the AMs were detected using reverse transcription-polymerase chain reaction (RT-PCR). The results revealed that a considerable number of inflammatory cells had infiltrated into the alveolar cavity in the BLM group at day 7, and less alveolitis and more serious fibrosis were observed at day 28, as compared with the NS group. Furthermore, when compared with the NS group, the protein expression levels of IL-17A in the lung tissue were markedly higher in the BLM group at days 7 and 28 (higher at day 7; P<0.05). In addition, the total number of BALF cells in the BLM group was clearly higher at day 7 when compared with the NS group (P<0.05), although a normal level was re-established by day 28. The level of IL-17A in the BALF increased significantly at days 7 and 28 in the BLM group; however, when compared with the level at day 7, the concentration had decreased at day 28. When compared with the NS group, the protein expression levels of IL-17A in the BLM group were notably higher after 12, 24 and 48 h. In addition, the results of the RT-PCR assay revealed that the mRNA expression levels of IL-17A increased significantly at days 7 and 28 in the BLM group when compared with the NS group (P<0.05). Therefore, IL-17A was demonstrated to promote the development of pulmonary inflammation, which may be involved in the development of pulmonary fibrosis.
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