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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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The Th17 response promotes the accumulation of inflammatory cells in BALF. Total cells (A), neutrophils (B), lymphocytes (C) and macrophages (D) in BALF were counted using Giemsa staining (n = 4). Results are represented as means ± SEM (*P < 0.05 versus the control Ab + silica group).
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fig05: The Th17 response promotes the accumulation of inflammatory cells in BALF. Total cells (A), neutrophils (B), lymphocytes (C) and macrophages (D) in BALF were counted using Giemsa staining (n = 4). Results are represented as means ± SEM (*P < 0.05 versus the control Ab + silica group).

Mentions: To assess the function of the IL-17/Th17 response in the inflammatory stage of silicosis, we examined the lung response to IL-17 neutralization. An anti-IL-17 mAb effectively neutralized IL-17 in the lung on days 1 and 4, significantly at day 4 (P < 0.05; Fig. 4A). Th17 cells in the spleen were decreased significantly in the anti-IL-17 mAb+silica group compared with Th17 cells in the control Ab+silica group (P < 0.05; Fig. 4B). These results demonstrated neutralization of IL-17 in mice treated with an anti-IL-17 mAb. Silica-induced lung inflammation was limited in the group administered anti-IL-17 mAb compared with mice administered control Ab (Fig. 4C). We then examined the accumulation of inflammatory cells (i.e., total cells, neutrophils, lymphocytes and macrophages) in BALF. Neutralization of IL-17 downregulated the total cell numbers in BALF significantly on days 1 and 4 (P < 0.05; Fig. 5A). Neutrophils in the anti-IL-17 mAb + silica group decreased significantly compared with those in the saline + silica group on days 1 and 4 (P < 0.05; Fig. 5B). Lymphocytes and macrophages in the anti-IL-17 mAb+silica group both decreased to varying degrees (Fig. 5C and D). These results support key functions for IL-17/Th17 in the development of lung inflammation in silicosis.


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)

The Th17 response promotes the accumulation of inflammatory cells in BALF. Total cells (A), neutrophils (B), lymphocytes (C) and macrophages (D) in BALF were counted using Giemsa staining (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

fig05: The Th17 response promotes the accumulation of inflammatory cells in BALF. Total cells (A), neutrophils (B), lymphocytes (C) and macrophages (D) in BALF were counted using Giemsa staining (n = 4). Results are represented as means ± SEM (*P < 0.05 versus the control Ab + silica group).
Mentions: To assess the function of the IL-17/Th17 response in the inflammatory stage of silicosis, we examined the lung response to IL-17 neutralization. An anti-IL-17 mAb effectively neutralized IL-17 in the lung on days 1 and 4, significantly at day 4 (P < 0.05; Fig. 4A). Th17 cells in the spleen were decreased significantly in the anti-IL-17 mAb+silica group compared with Th17 cells in the control Ab+silica group (P < 0.05; Fig. 4B). These results demonstrated neutralization of IL-17 in mice treated with an anti-IL-17 mAb. Silica-induced lung inflammation was limited in the group administered anti-IL-17 mAb compared with mice administered control Ab (Fig. 4C). We then examined the accumulation of inflammatory cells (i.e., total cells, neutrophils, lymphocytes and macrophages) in BALF. Neutralization of IL-17 downregulated the total cell numbers in BALF significantly on days 1 and 4 (P < 0.05; Fig. 5A). Neutrophils in the anti-IL-17 mAb + silica group decreased significantly compared with those in the saline + silica group on days 1 and 4 (P < 0.05; Fig. 5B). Lymphocytes and macrophages in the anti-IL-17 mAb+silica group both decreased to varying degrees (Fig. 5C and D). These results support key functions for IL-17/Th17 in the development of lung inflammation in silicosis.

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