The findings could lead to new ways to prevent or treat early lung changes leading to the disease. The tiny, breathable Fine Particulate matter (FPM), found in air pollutants, has been identified as a group 1 carcinogen and a major threat to global health. However, the cause of FPM’s cancer remains unclear.
“Despite its transformational power, recent research shows that FPM does not directly stimulate – and may inhibit – the growth of lung cancer cells,” explains first author Zhenzhen Wang, a joint researcher at Nanjing University (NJU), Nanjing. , China, who conducted research between NJU labs and the University of Macau where they were sponsored by the University of Macau Fellowship. “This suggests that FPM may lead to cancer through indirect mechanisms that support tumor growth. For example, some studies suggest that FPM may prevent immune cells from moving where they need to be.”
To test this possibility, Wang and team collected FPM at seven locations in China and studied its effects on the main growth cells of the tumor – called cytotoxic T-cells (CTLs). In mice controlled by lung cancer cells that were not exposed to FPM, CTLs were collected in the lungs to destroy tumor cells. In contrast, in mice whose lungs were exposed to FPM, CTL infiltration was delayed – possibly allowing tumor cells to form in the lung tissue.
To investigate why CTLs did not immediately enter the lungs in the lungs that emerged from FPM, the team studied both CTLs themselves and lung tissue structure. They found that the CTLs exposed to FPM still retained their ability to migrate, but that exposure to FPM dramatically suppressed lung tissue formation and the space between the immune cells. There were also very high levels of collagen – a protein that provides biomechanical support to cells and tissues. While the team monitored the CTL movement in mice, the lung trap exposed to FPM, CTLs struggled to move, and those with untreated tissue were able to move more freely.
Further tissue analysis showed that structural changes were caused by an increase in collagen subtype called collagen IV, but the team did not know how FPM started this. They found the answer when they took a closer look at the structural changes in collagen IV and the enzyme responsible for it – called peroxidasin. This enzyme triggers a specific type of link that is found that exposure to FPM causes and exacerbates lung tissue.
“The most surprising finding was the way this process took place,” Wang said. “The enzyme peroxidasin is attached to FPM in the lungs, which increases its activity. When combined, this means that wherever FPM reaches the lungs, an increase in peroxidasin activity leads to a change in the structure of the lung tissue that can keep the body cells outside and far away. tumor cells. “
“Our research reveals a whole new way of inhaling fine-grained particles that promote lung growth,” concludes lead author Lei Dong, professor at the School of Life Sciences, at Nanjing University. “We provide direct evidence that proteins adhere to the matter of good molecules can cause significant and negative effects, resulting in pathogenic activity.
Source Journal Reference: Zhenzhen Wang, Ziyu Zhai, Chunyu Chen, Xuejiao Tian, Zhen Xing, Panfei Xing, Yushun Yang, Junfeng Zhang, Chunming Wang, Lei Dong. Air pollution particles hijack peroxidasin to disrupt immunosurveillance and promote lung cancer. eLife, 2022; 11 DOI: 10.7554/eLife.75345
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