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Mengtian XIA, Beilei LI, Qian CHEN, Xiafei JIN, Feng WEI, Kaixuan WANG. The Effect of Microbial Metabolites on Immune Function Reconstruction of Aids Based on Mitochondrial Dysfunction[J]. Journal of Kunming Medical University.
Citation: Mengtian XIA, Beilei LI, Qian CHEN, Xiafei JIN, Feng WEI, Kaixuan WANG. The Effect of Microbial Metabolites on Immune Function Reconstruction of Aids Based on Mitochondrial Dysfunction[J]. Journal of Kunming Medical University.

The Effect of Microbial Metabolites on Immune Function Reconstruction of Aids Based on Mitochondrial Dysfunction

  • Received Date: 2025-06-11
  •   objective  To explore the effect of microbial metabolites on immune function reconstruction of AIDS based on mitochondrial dysfunction.   Methods  From October 2023 to March 2024, 42 HIV-infected people who received antiretroviral therapy (ART) for 4 years were recruited, including 20 immune non-responders (INR) and 22 responders (IR). At the same time, 20 non-infected MSM matched by sex and age were selected as the control group, and their HIV, hepatitis B or hepatitis C virus infection were all negative. The immune parameters were analyzed by flow cytometry. The levels of free fatty acid (FFA) and ferrous (Fe2+) in plasma were determined by fluorescence assay kit and iron colorimetric assay kit.   Results  The percentages of CD4+ T cells, CD4+CD45RA+ T cells and CD4+CD45RA+CD31+ T cells in INR group were lower than those in control group and IR group (P < 0.05). Compared with IR group, the JC-1 ratio of CD4+ T cells, the level of reactive oxygen species (ROS) and the peroxidation/antioxidation of C11-BODIPY in INR group increased (P < 0.05). The lipid ROS level of CD4+ T cells in IR group was higher than that in control group (P < 0.05). The FFA level and Fe2+ level in peripheral blood of patients in INR group were higher than those in control group and IR group (P < 0.05), and the percentage of CD4+CD36+ T cells was lower than that in control group and IR group (P < 0.05), but there was no significant difference between control group and IR group.   Conclusion  The increase of FFA, a metabolite of flora, is accompanied by the decrease of CD36 receptor expression on CD4+ T cells, leading to mitochondrial dysfunction.
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