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Exogenous Gas6 attenuates silica-induced inflammation on differentiated THP-1 macrophages
Yan Shen1, Xiuqing Cui1, Yi Rong1
1Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Abstract:
Growth arrest specific 6 (Gas6) has been reported to be related to the modulation of innate immunity. To investigate the potential effect of Gas6 on the regulation of inflammations induced by silica, differentiated THP-1 macrophages were exposed to different concentrations of silica for 6h and 24h. Additionally, silica-activated macrophages were treated with Gas6 antibody and Gas6 respectively. Expression levels of Gas6 and inflammatory cytokines (TNF-α, IL-1β and IL-6) were measured. Our results showed that both cell viability and Gas6 expression were suppressed by silica in dose-dependent manners. After pretreatment with Gas6 antibody, silica induced a significant decrease in cell viability and a significant increase in inflammatory cytokines at two time points. Moreover, addition of Gas6 significantly suppressed silica induced TNF-α, IL-1β and IL-6 levels in negative dose-dependent manners, not only in mRNA levels but also in protein levels. Our results suggested that exogenous Gas6 might attenuate inflammations induced by silica on macrophages.
Insights
Growth arrest specific 6 (Gas6) may protect against silica-induced inflammation in macrophages. Adding Gas6 reduced inflammatory cytokines, while blocking Gas6 worsened silica
Area of Science:
- Immunology
- Cell Biology
- Toxicology
Background:
- Growth arrest specific 6 (Gas6) is implicated in modulating innate immunity.
- Silica exposure can trigger inflammatory responses in macrophages.
Purpose of the Study:
- To investigate the role of Gas6 in silica-induced inflammation.
- To determine if Gas6 can attenuate silica-induced inflammatory responses in macrophages.
Main Methods:
- THP-1 macrophages were exposed to silica and treated with Gas6 antibody or Gas6.
- Cell viability, Gas6 expression, and inflammatory cytokine levels (TNF-α, IL-1β, IL-6) were measured at mRNA and protein levels.
Main Results:
- Silica suppressed cell viability and Gas6 expression in a dose-dependent manner.
- Gas6 antibody treatment exacerbated silica-induced inflammation and decreased cell viability.
- Exogenous Gas6 significantly suppressed silica-induced inflammatory cytokine production.
Conclusions:
- Gas6 plays a protective role against silica-induced inflammation in macrophages.
- Exogenous Gas6 demonstrates potential as an anti-inflammatory agent in silica exposure models.
