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Research
1,4NQ-BC enhances the lung inflammation by mediating the secretion of IL-33 which derived from macrophages
Xuetao Wei
School of Public Health, Peking University
Corresponding Author
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This work is licensed under a CC BY 4.0 License. Read Full License
Background Black carbon (BC) is a product of incomplete combustion of fossil fuels and vegetation. The compelling evidence has demonstrated that it has a close relationship with several respiratory and cardiovascular diseases. BC provides the reactive sites and surfaces to absorb various chemicals, such as polycyclic aromatic hydrocarbons (PAH). Naphthoquinone is a typical PAHs which was found in particulate matter (PM) and 1,4NQ-BC owned high oxidative potential and cytotoxicity. IL-33 is an alarmin which increases innate immunity through Th2 responses. It was reported that IL-33 was a potent inducer of pro-inflammatory cytokines, like IL-6. In our previous study, it was revealed that 1,4NQ-BC instilled intratracheally to mice could trigger zthe lung inflammation and stimulate the secretion of IL-33 in lung tissue.
Results We found that IL-33 could induce inflammation in lung itself. When the macrophages were eliminated, the secretion of IL-33 was reduced and the pathological damage in the lung was relieved after exposure to 1,4NQ-BC. Both MAPK and PI3k/Akt signal pathways were involved in the process of IL-33 secretion and the lung inflammation induced by 1,4NQ-BC.
Conclusions The findings herein support the notion that after exposure to 1,4NQ-BC, the increased secretion of IL-33 was mainly derived from macrophage through both MAPK and PI3k/Akt signal pathways.
Keywords
IL-33, 1,4NQ-BC, lung inflammation, macrophage
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This is a preprint. It has not completed peer review.
Research
1,4NQ-BC enhances the lung inflammation by mediating the secretion of IL-33 which derived from macrophages
Xuetao Wei
School of Public Health, Peking University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 02 Jan, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background Black carbon (BC) is a product of incomplete combustion of fossil fuels and vegetation. The compelling evidence has demonstrated that it has a close relationship with several respiratory and cardiovascular diseases. BC provides the reactive sites and surfaces to absorb various chemicals, such as polycyclic aromatic hydrocarbons (PAH). Naphthoquinone is a typical PAHs which was found in particulate matter (PM) and 1,4NQ-BC owned high oxidative potential and cytotoxicity. IL-33 is an alarmin which increases innate immunity through Th2 responses. It was reported that IL-33 was a potent inducer of pro-inflammatory cytokines, like IL-6. In our previous study, it was revealed that 1,4NQ-BC instilled intratracheally to mice could trigger zthe lung inflammation and stimulate the secretion of IL-33 in lung tissue.
Results We found that IL-33 could induce inflammation in lung itself. When the macrophages were eliminated, the secretion of IL-33 was reduced and the pathological damage in the lung was relieved after exposure to 1,4NQ-BC. Both MAPK and PI3k/Akt signal pathways were involved in the process of IL-33 secretion and the lung inflammation induced by 1,4NQ-BC.
Conclusions The findings herein support the notion that after exposure to 1,4NQ-BC, the increased secretion of IL-33 was mainly derived from macrophage through both MAPK and PI3k/Akt signal pathways.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7