Neutralization of interleukin-17A delays progression of silica-induced lung inflammation and fibrosis in C57BL/6 mice

Dec 3, 2013Toxicology and applied pharmacology

Blocking interleukin-17A slows lung inflammation and scarring caused by silica in mice

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Abstract

IL-17A neutralization delayed neutrophil accumulation and progression of silica-induced lung inflammation and fibrosis.

Neutralization of IL-17A reduced the percentage of Th17 cells in CD4+ T cells during silica exposure.
Decreased levels of IL-6 and IL-1β were observed following IL-17A neutralization.
An increase in regulatory T cells (Tregs) was noted at an early stage of silica-induced inflammation.
IL-17A neutralization also delayed the Th1/Th2 immune response during silica-induced inflammation and fibrosis.
These findings indicate that IL-17A may play a pivotal role in the early phase of silica-induced inflammation.

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Silica exposure can cause lung inflammation and fibrosis, known as silicosis. Interleukin-17A (IL-17A) and Th17 cells play a pivotal role in controlling inflammatory diseases. However, the roles of IL-17A and Th17 cells in the progress of silica-induced inflammation and fibrosis are poorly understood. This study explored the effects of IL-17A on silica-induced inflammation and fibrosis. We used an anti-mouse IL-17A antibody to establish an IL-17A-neutralized mice model, and mice were exposed to silica to establish an experimental silicosis model. We showed that IL-17A neutralization delayed neutrophil accumulation and progression of silica-induced lung inflammation and fibrosis. IL-17A neutralization reduced the percentage of Th17 in CD4+ T cells, decreased IL-6 and IL-1β expression, and increased Tregs at an early phase of silica-induced inflammation. Neutralization of IL-17A delayed silica-induced Th1/Th2 immune and autoimmune responses. These results suggest that IL-17A neutralization alleviates early stage silica-induced lung inflammation and delays progression of silica-induced lung inflammation and fibrosis. Neutralization of IL-17A suppressed Th17 cell development by decreasing IL-6 and/or IL-1β and increased Tregs at an early phase of silica-induced inflammation. Neutralization of IL-17A also delayed the Th1/Th2 immune response during silica-induced lung inflammation and fibrosis. IL-17A may play a pivotal role in the early phase of silica-induced inflammation and may mediate the Th immune response to influence silica-induced lung inflammation and fibrosis in mice.

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