MLE12 및 RAW264.7세포에서 Alternaria와 Alternariol Mycotoxin의 알레르기 염증반응 효과
Alternaria and Alternariol Mycotoxins Affect Production of Allergic Inflammatory Cytokines in MLE12 and RAW264.7 Cells
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Background: Alternaria and their secondary metabolites, alternariol mycotoxins, may cause respiratory symptoms and asthma. Moreover, microbial compounds, such as bacterial endotoxins, act as potential contributors in such situations. Alveolar epithelial cells and macrophages appear to initiate airway inflammation through proinflammatory cytokines after exposure to aeroallergens or toxic materials. The present study investigated the effects of Alternaria and alternariol mycotoxins on inflammatory cytokines secreted from airway epithelial cells and macrophages, especially interleukin-33,interleukin-6 and tumor necrosis factor-α, which were assessed association with lipopolysaccharide. Methods: In vitro MLE12 cells and RAW264.7 cells were treated with Alternaria, alternariol monomethyl ether and alternariol at different doses for 24 hour. The levels of interleukin-33, interleukin-6, and tumor necrosis factor-α in each cell supernatants were measured by ELISA. Then, each mycotoxin (100 ng/mL) was added to lipopolysaccharide stimulated cells and incubated with them. Cell viability was measured by flow cytometry. Results: Alternaria and alternariol mycotoxin-treated cells released pro-inflammatory cytokines partly in a dose-dependent manner. Moreover, lipopolysaccharide induced the synergic effect of mycotoxins on cytokine production by RAW264.7 cells. However, the different cytokine productions among groups were not related to cell viability. Conclusion: This study suggests that alternariol mycotoxins,such as Alternaria, would provoke airway inflammation through interleukin-33, interleukin-6 and tumor necrosis factor-α uction from epithelial cells and macrophages.
Abstract
Background: Alternaria and their secondary metabolites, alternariol mycotoxins, may cause respiratory symptoms and asthma. Moreover, microbial compounds, such as bacterial endotoxins, act as potential contributors in such situations. Alveolar epithelial cells and macrophages appear to initiate airway inflammation through proinflammatory cytokines after exposure to aeroallergens or toxic materials. The present study investigated the effects of Alternaria and alternariol mycotoxins on inflammatory cytokines secreted from airway epithelial cells and macrophages, especially interleukin-33,interleukin-6 and tumor necrosis factor-α, which were assessed association with lipopolysaccharide. Methods: In vitro MLE12 cells and RAW264.7 cells were treated with Alternaria, alternariol monomethyl ether and alternariol at different doses for 24 hour. The levels of interleukin-33, interleukin-6, and tumor necrosis factor-α in each cell supernatants were measured by ELISA. Then, each mycotoxin (100 ng/mL) was added to lipopolysaccharide stimulated cells and incubated with them. Cell viability was measured by flow cytometry. Results: Alternaria and alternariol mycotoxin-treated cells released pro-inflammatory cytokines partly in a dose-dependent manner. Moreover, lipopolysaccharide induced the synergic effect of mycotoxins on cytokine production by RAW264.7 cells. However, the different cytokine productions among groups were not related to cell viability. Conclusion: This study suggests that alternariol mycotoxins,such as Alternaria, would provoke airway inflammation through interleukin-33, interleukin-6 and tumor necrosis factor-α uction from epithelial cells and macrophages.
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