eLife: NTU Dong Lei's team and others reveal a new mechanism by which haze and cigarette particles aggravate lung cancer

Epidemiological studies have shown that the long-term exposure of PM5, PM1, and fine inhalable particulate matter (FPM) such as cigarette smoke particles in haze is closely related to the occurrence ^of lung canc.

At present, the research on the carcinogenicity of FPM mainly focuses on the gene mutation induced by particulate matt.

Recently, the team of Professor Dong Lei and Professor Zhang Junfeng from the State Key Laboratory of Medical Biotechnology (School of Life Sciences) of Nanjing University, together with the team of Wang Chunming from the University of Macau, published an online publication titled: Air Pollution Particles Hijack Peroxidasin to Disrupt Immunosurveillance and Promote Lung Cancer in eLi.

The study revealed a new mechanism by which haze and cigarette particles exacerbate lung canc.

First, the authors analyzed the correlation between lung cancer development and early immune defense in the lungs after exposure to fine particulate matter (FP.

Next, the study analyzed how FPM interfered with the infiltration and killing activity of local CTLs in lung tiss.

FigureInhalable fine particulate matter (including haze particles PM1 and cigarette smoke particles TSP) can increase the degree of collagen cross-linking in lung tissue (A and B) and inhibit T cell migration (C)

FigureSchematic diagram of the overall stu.

FigureRespirable fine particles (PM1 and TSP) participate in collagen cross-linking (A) via biomacromolecular activity at the "material-bio" interface, enhancing the formation of sulfimide bonds (-S=N-) at the cross-linking site (B)

FigureRespirable fine particles induce phase separation of the enzyme PXDN, which specifically catalyzes the formation of -S=N-, and promotes the transition of the enzyme from a free state to an aggregated state (A and .

Original source:

Zhenzhen Wang, Ziyu Zhai, Chunyu Chen, et .