title: Reduction of IL-17A might suppress the Th1 response and promote the Th2 response by boosting the function of Treg cells during silica-induced inflammatory response in vitro.
abstract: Silica inhalation can induce chronic lung inflammation and fibrosis. Upon silica stimulation, activated macrophages trigger the T-lymphocyte which can differentiate into many different types of Th cells, including the recently discovered Th17 cells. IL-17A, the typical Th17 cytokine, is reported in some inflammatory diseases. However, the role of IL-17A in silica-induced inflammatory response is still not clear. The regulatory mechanism of silica-induced Th17 response also needs to be investigated. So we established a mice primary cell coculture system (macrophage and lymphocyte) to investigate the role of IL-17A in silica-induced inflammatory response in vitro, by using anti-IL-17A mAb and IL-1Ra. Both anti-IL-17A mAb and IL-1Ra decreased the level of IL-17A and increased the function of Treg cells. The Th1 response was suppressed and the Th2 response was promoted by the addition of anti-IL-17A mAb or IL-1Ra. IL-1Ra treatment decreased the level of IL-6, whereas the levels of IL-23 and ROR- γ t were increased. Our study demonstrated that IL-17A reduction altered the pattern of silica-induced Th responses by boosting the function of Treg cells in vitro. Blocking the function of IL-1 signal pathway could suppress the level of IL-17A, which played the major role in modulating silica-induced Th responses in vitro.
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Wen
authors.initials: W
authors.lastname: Tang
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Fangwei
authors.initials: F
authors.lastname: Liu
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Laiyu
authors.initials: L
authors.lastname: Song
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Wujing
authors.initials: W
authors.lastname: Dai
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Li
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Weng
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, No. 92 North 2nd Road, Heping District, Shenyang, Liaoning 110001, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid; D002454:Cell Differentiation; D018920:Coculture Techniques; D005260:Female; D005786:Gene Expression Regulation; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology; D020381:Interleukin-17 / Q000502:physiology*; D053759:Interleukin-23 / Q000378:metabolism; D008214:Lymphocytes / Q000166:cytology; D008264:Macrophages / Q000166:cytology; D051379:Mice; D008810:Mice, Inbred C57BL; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000378:metabolism; D053573:Receptors, Interleukin-1 Type I / Q000378:metabolism; D015398:Signal Transduction; D012822:Silicon Dioxide / Q000737:chemistry*; D050378:T-Lymphocytes, Regulatory / Q000166:cytology*; D018417:Th1 Cells / Q000166:cytology*; D018418:Th2 Cells / Q000166:cytology*
chemical_list: D000911:Antibodies, Monoclonal; C583355:IL1R1 protein, mouse; C098680:Il17a protein, mouse; D020381:Interleukin-17; D053759:Interleukin-23; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D053573:Receptors, Interleukin-1 Type I; C539901:Rorc protein, mouse; D012822:Silicon Dioxide