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Th17 can regulate silica-induced lung inflammation through an IL-1β-dependent mechanism.

Song L, Weng D, Dai W, Tang W, Chen S, Li C, Chen Y, Liu F, Chen J - J. Cell. Mol. Med. (2014)

Bottom Line: The Th17 response, which is induced by IL-1β, has been reported very important in chronic human lung inflammatory diseases.Treatment with an IL-1 type I receptor (IL-1RI) antagonist anakinra substantially decreased silica-induced lung inflammation and the Th17 response.Silica may induce IL-1β production from alveolar macrophages and promote inflammation by initiating a Th17 response via an IL-1β/IL-1RI-dependent mechanism.

View Article: PubMed Central - PubMed

Affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China; Department of Clinical Immunology, Dalian Medical University, Dalian, China.

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IL-17 may regulate silica-induced lung inflammation by modulating the Th immune balance. The levels of T-bet (A) and Foxp3 mRNA (D) in the spleen were assayed by real-time RT-PCR using the −ΔΔCt method (n = 4). Th1 cells in the spleen (B and G) and hilar lymph nodes (HLNs; C) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (B and C; n = 4). Tregs in the spleen (E and G) and HLNs (F) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (E and F; n = 4). Results are represented as means ± SEM (*P < 0.05 versus the control Ab + silica group)).
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fig06: IL-17 may regulate silica-induced lung inflammation by modulating the Th immune balance. The levels of T-bet (A) and Foxp3 mRNA (D) in the spleen were assayed by real-time RT-PCR using the −ΔΔCt method (n = 4). Th1 cells in the spleen (B and G) and hilar lymph nodes (HLNs; C) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (B and C; n = 4). Tregs in the spleen (E and G) and HLNs (F) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (E and F; n = 4). Results are represented as means ± SEM (*P < 0.05 versus the control Ab + silica group)).

Mentions: The Th immune response is very important in the progress of lung inflammation [22]. The massive expansion of the Th17 cell population can create an imbalance between effector T cells (such as Th1 cells) and regulatory T cells (Tregs), which determine the outcome of adaptive immune responses [23]. We assessed the effects of IL-17 on the T cell immune response to test whether IL-17 could promote the lung inflammation of silicosis by influencing related immune responses. We examined T-bet, the key transforming growth factor of Th1 cells. IL-17 neutralization significantly increased T-bet mRNA expression in our silicosis model on days 4 and 11 (P < 0.05; Fig. 6A). CD4+IFN-γ+ Th1 cells in the spleen were increased significantly in the anti-IL-17 mAb+silica group compared with those in the control Ab + silica group on day 11 (P < 0.05; Fig. 6B). In the HLNs of anti-IL-17 mAb + silica-treated mice, CD4+IFN-γ+ Th1 cells were significantly increased in the anti-IL-17 mAb + silica group compared with those in the control Ab + silica group on days 1 and 4 (P < 0.05; Fig. 6C). These data suggest that the Th1 immune response is increased in the silicosis mouse model treated with anti-IL-17 mAb.


Th17 can regulate silica-induced lung inflammation through an IL-1β-dependent mechanism.

Song L, Weng D, Dai W, Tang W, Chen S, Li C, Chen Y, Liu F, Chen J - J. Cell. Mol. Med. (2014)

IL-17 may regulate silica-induced lung inflammation by modulating the Th immune balance. The levels of T-bet (A) and Foxp3 mRNA (D) in the spleen were assayed by real-time RT-PCR using the −ΔΔCt method (n = 4). Th1 cells in the spleen (B and G) and hilar lymph nodes (HLNs; C) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (B and C; n = 4). Tregs in the spleen (E and G) and HLNs (F) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (E and F; n = 4). Results are represented as means ± SEM (*P < 0.05 versus the control Ab + silica group)).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4196653&req=5

fig06: IL-17 may regulate silica-induced lung inflammation by modulating the Th immune balance. The levels of T-bet (A) and Foxp3 mRNA (D) in the spleen were assayed by real-time RT-PCR using the −ΔΔCt method (n = 4). Th1 cells in the spleen (B and G) and hilar lymph nodes (HLNs; C) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (B and C; n = 4). Tregs in the spleen (E and G) and HLNs (F) were calculated by flow cytometry, and the percentage of CD4 + IFN-γ+ T cells was plotted (E and F; n = 4). Results are represented as means ± SEM (*P < 0.05 versus the control Ab + silica group)).
Mentions: The Th immune response is very important in the progress of lung inflammation [22]. The massive expansion of the Th17 cell population can create an imbalance between effector T cells (such as Th1 cells) and regulatory T cells (Tregs), which determine the outcome of adaptive immune responses [23]. We assessed the effects of IL-17 on the T cell immune response to test whether IL-17 could promote the lung inflammation of silicosis by influencing related immune responses. We examined T-bet, the key transforming growth factor of Th1 cells. IL-17 neutralization significantly increased T-bet mRNA expression in our silicosis model on days 4 and 11 (P < 0.05; Fig. 6A). CD4+IFN-γ+ Th1 cells in the spleen were increased significantly in the anti-IL-17 mAb+silica group compared with those in the control Ab + silica group on day 11 (P < 0.05; Fig. 6B). In the HLNs of anti-IL-17 mAb + silica-treated mice, CD4+IFN-γ+ Th1 cells were significantly increased in the anti-IL-17 mAb + silica group compared with those in the control Ab + silica group on days 1 and 4 (P < 0.05; Fig. 6C). These data suggest that the Th1 immune response is increased in the silicosis mouse model treated with anti-IL-17 mAb.

Bottom Line: The Th17 response, which is induced by IL-1β, has been reported very important in chronic human lung inflammatory diseases.Treatment with an IL-1 type I receptor (IL-1RI) antagonist anakinra substantially decreased silica-induced lung inflammation and the Th17 response.Silica may induce IL-1β production from alveolar macrophages and promote inflammation by initiating a Th17 response via an IL-1β/IL-1RI-dependent mechanism.

View Article: PubMed Central - PubMed

Affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China; Department of Clinical Immunology, Dalian Medical University, Dalian, China.

Show MeSH
Related in: MedlinePlus