• How air pollution alters lung tissue, in

    From ScienceDaily@1:317/3 to All on Tue Apr 19 22:30:44 2022
    How air pollution alters lung tissue, increasing cancer susceptibility


    Date:
    April 19, 2022
    Source:
    eLife
    Summary:
    Scientists have identified a mechanism that explains how fine
    air pollution particles might cause lung cancer, according to a
    new study.



    FULL STORY ========================================================================== Scientists have identified a mechanism that explains how fine air
    pollution particles might cause lung cancer, according to a study
    published today in eLife.


    ==========================================================================
    The findings could lead to new approaches for preventing or treating
    the initial lung changes that lead to the disease.

    Tiny, inhalable fine particulate matter (FPM) found in air pollutants
    has been recognised as a Group 1 carcinogen and a substantial threat to
    global health.

    However, the cancer-causing mechanism of FPM remains unclear.

    "Despite its potential to cause mutations, recent research suggests that
    FPM does not directly promote -- and may even inhibit -- the growth of
    lung cancer cells," explains first author Zhenzhen Wang, an associate researcher at Nanjing University (NJU), Nanjing, China, who carried
    out the study between labs at NJU and the University of Macau where she
    was sponsored by a University of Macau Fellowship. "This suggests that
    FPM might lead to cancer through indirect means that support tumour
    growth. For example, some studies suggest FPM can prevent immune cells
    from moving to where they are needed." To explore this possibility, Wang
    and the team collected FPM from seven locations in China and studied its effects on the main immune cells that defend against tumour growth --
    called cytotoxic T-cells (CTLs). In mice administered with lung cancer
    cells that were not exposed to FPM, CTLs were recruited to the lung to
    destroy the tumour cells. By contrast, in the mice whose lungs were
    exposed to FPM, the infiltration of CTLs was delayed -- potentially
    allowing the tumour cells to establish in lung tissue.

    To investigate why the CTLs did not enter the lung as quickly in the
    FPM- exposed lungs, the team studied both the CTLs themselves and
    the lung tissue structure. They found that CTLs exposed to FPM still
    retained their migratory ability, but that FPM exposure dramatically
    compressed the lung tissue structure and the spaces that immune cells
    move between. There were also much higher levels of collagen -- a protein
    that provides biomechanical support for cells and tissues. When the team studied the movement of CTLs in the mice, in lung tissue exposed to FPM,
    CTLs struggled to move, whereas those in the untreated tissue were able
    to move freely.

    Further analysis of the tissue showed that the structural changes were
    caused by increases in a collagen subtype called collagen IV, but the
    team still did not know how FPM triggered this. They found the answer
    when they looked more closely at the structural changes to collagen IV
    and the enzyme responsible for making them -- called peroxidasin. This
    enzyme drives a specific type of cross- linking that exposure to FPM
    was found to cause and aggravate in the lung tissue.

    "The most surprising find was the mechanism by which this process
    occurred," Wang says. "The peroxidasin enzyme stuck to the FPM in
    the lung, which increased its activity. Taken together, this means
    that wherever FPM lands in the lung, increased peroxidasin activity
    leads to structural changes in the lung tissue that can keep immune
    cells out and away from growing tumour cells." "Our study reveals a
    completely new mechanism by which inhaled fine particles promote lung
    tumour development," concludes senior author Lei Dong, Professor at
    the School of Life Sciences, Nanjing University. "We provide direct
    evidence that proteins that stick to fine particulate matter can cause a significant and adverse effect, giving rise to pathogenic activity. Our discovery that peroxidasin is the mediator of this effect in lung tissue identifies it as a specific and unexpected target for preventing lung
    disease caused by air pollution."

    ========================================================================== Story Source: Materials provided by eLife. Note: Content may be edited
    for style and length.


    ========================================================================== Journal Reference:
    1. 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 ==========================================================================

    Link to news story: https://www.sciencedaily.com/releases/2022/04/220419112520.htm

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