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<p><i>Mycobacterium bovis</i> (<i>M. bovis</i>) is a major pathogen that causes zoonotic tuberculosis. It is transmitted via aerosols, colonizes the lungs of the host and causes oxidative stress in macrophages, resulting in tissue damage. The mechanisms underlying the oxidative damage to cells induced by this infection have not yet been fully elucidated. This study investigated the effects of SH3PXD2B on the production of reactive oxygen species (ROS) and antioxidant mechanisms during <i>M. bovis</i> infection. The results showed that SH3PXD2B expression was significantly upregulated after <i>M. bovis</i> infection, and promoted the production of cellular NOX-dependent ROS and the lipid peroxidation marker MDA. Additionally, overexpression of SH3PXD2B inhibited the Nrf2 antioxidant pathway and reduced the activities of antioxidant enzymes such as CAT, SOD, and GPx. Conversely, knockdown of SH3PXD2B exerted the opposite effect and improved cell viability. In summary, SH3PXD2B orchestrates <i>M. bovis</i>-induced oxidative stress in macrophages through a dual mechanism: amplifying ROS production while simultaneously crippling the host’s antioxidant capacity. These findings provide novel mechanistic insights into <i>M. bovis</i> pathogenesis and suggest that SH3PXD2B may be a potential molecular target for future research into disease resistance in cattle and the development of new therapies.</p>

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Mycobacterium bovis induces cellular oxidative stress via the host protein SH3PXD2B

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月3日

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  • Donghui Liu,
  • Ting Zhang,
  • Zhengzhong Xu,
  • Chengkun Zheng,
  • Xin’an Jiao,
  • Xiang Chen

摘要

Mycobacterium bovis (M. bovis) is a major pathogen that causes zoonotic tuberculosis. It is transmitted via aerosols, colonizes the lungs of the host and causes oxidative stress in macrophages, resulting in tissue damage. The mechanisms underlying the oxidative damage to cells induced by this infection have not yet been fully elucidated. This study investigated the effects of SH3PXD2B on the production of reactive oxygen species (ROS) and antioxidant mechanisms during M. bovis infection. The results showed that SH3PXD2B expression was significantly upregulated after M. bovis infection, and promoted the production of cellular NOX-dependent ROS and the lipid peroxidation marker MDA. Additionally, overexpression of SH3PXD2B inhibited the Nrf2 antioxidant pathway and reduced the activities of antioxidant enzymes such as CAT, SOD, and GPx. Conversely, knockdown of SH3PXD2B exerted the opposite effect and improved cell viability. In summary, SH3PXD2B orchestrates M. bovis-induced oxidative stress in macrophages through a dual mechanism: amplifying ROS production while simultaneously crippling the host’s antioxidant capacity. These findings provide novel mechanistic insights into M. bovis pathogenesis and suggest that SH3PXD2B may be a potential molecular target for future research into disease resistance in cattle and the development of new therapies.