title: T(reg) cells may regulate interlukin-17 production by modulating TH1 responses in 1,3-β-glucan-induced lung inflammation in mice.
abstract: 1,3-β-glucan is considered a fungal biomarker and exposure to this agent can induce lung inflammation. Complement activation plays an important role in early immune responses to β-glucan. Previous studies showed that T-regulatory cells (Tregs) regulated 1,3-β-glucan-induced lung inflammation by modulating the maintenance of immune homeostasis in the lung. Both interleukin (IL)-17 and TH17 cells play pivotal roles in inflammation associated with lung disease and share reciprocal developmental pathways with Tregs. However, the effect of Tregs on IL-17 and TH17 responses in 1,3-β-glucan-induced lung inflammation remains unclear. In this study, mice were exposed to 1,3-β-glucan by intratracheal instillation. To investigate the effects of Tregs on IL-17 and TH17 cells in the induced lung inflammation, a Treg-depleted mice model was generated by administration of anti-CD25 mAb. The results indicated that Treg-depleted mice showed more severe pathological inflammatory changes in lung tissues. Tregs depletion reduced IL-17 expression in these tissues, and increased those of TH1 cytokines. The expression of IL-17 increased at the early phase of the inflammation response. There were no significant effects of the Tregs on expression of RORγt and IL-6 or the amount of CD4(+)IL-17(+) cells in the lungs. When taken together, the late phase of the 1,3-β-glucan-induced inflammatory response in the mice was primarily mediated by TH1 cytokines rather than IL-17. In contrast, the early phase of the inflammatory response might be mediated in part by IL-17 along with activated complement. Tregs might be required for IL-17 expression during the late phase inflammatory response in mice. The increased IL-17 mRNA observed during the 1,3-β-glucan induced inflammatory response were attributed to cells other than TH17 cells.
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, PR China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Fangwei
authors.initials: F
authors.lastname: Liu
authors.forename: Dong
authors.initials: D
authors.lastname: Weng
authors.forename: Laiyu
authors.initials: L
authors.lastname: Song
authors.forename: Cuiying
authors.initials: C
authors.lastname: Li
authors.forename: Wen
authors.initials: W
authors.lastname: Tang
authors.forename: Ye
authors.initials: Y
authors.lastname: Yu
authors.forename: Wujing
authors.initials: W
authors.lastname: Dai
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology*; D020381:Interleukin-17 / Q000096:biosynthesis / Q000276:immunology*; D008212:Lymphocyte Depletion; D051379:Mice; D011014:Pneumonia / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D015054:Zymosan / Q000633:toxicity*
chemical_list: D020381:Interleukin-17; D012333:RNA, Messenger; D015054:Zymosan