Deramaudt Therese B, Chehaitly Ahmad, Charrière Théo, Arnaud Julie, Bonay Marcel
U1179 INSERM, END-ICAP, UFR des Sciences de la Santé-Simone Veil, Université de Versailles Saint-Quentin-en-Yvelines, 78180 Montigny-le-Bretonneux, France.
Service de Physiologie-Explorations Fonctionnelles, Hôpital Ambroise Paré, Assistance Publique-Hôpitaux de Paris, 92100 Boulogne-Billancourt, France.
Antioxidants (Basel). 2023 Aug 30;12(9):1695. doi: 10.3390/antiox12091695.
The effects of repetitive magnetic stimulation (rMS) have predominantly been studied in excitable cells, with limited research in non-excitable cells. This study aimed to investigate the impact of rMS on macrophages, which are crucial cells in the innate immune defense. THP-1-derived macrophages subjected to a 5 min session of 10 Hz rMS exhibited increased Nrf2 activation and decreased Keap1 expression. We found that activation of the Nrf2 signaling pathway relied on rMS-induced phosphorylation of p62. Notably, rMS reduced the intracellular survival of in macrophages. Silencing Nrf2 using siRNA in THP-1-derived macrophages or utilizing Nrf2 knockout in alveolar macrophages abolished this effect. Additionally, rMS attenuated the expression of IL-1β and TNF-α inflammatory genes by and inhibited p38 MAPK activation. These findings highlight the capacity of rMS to activate the non-canonical Nrf2 pathway, modulate macrophage function, and enhance the host's defense against bacterial infection.
重复磁刺激（rMS）的效应主要在可兴奋细胞中进行了研究，而在非可兴奋细胞中的研究有限。本研究旨在探讨rMS对巨噬细胞的影响，巨噬细胞是先天免疫防御中的关键细胞。接受10 Hz rMS 5分钟刺激的THP-1衍生巨噬细胞表现出Nrf2激活增加和Keap1表达降低。我们发现Nrf2信号通路的激活依赖于rMS诱导的p62磷酸化。值得注意的是，rMS降低了巨噬细胞内的存活率。在THP-1衍生巨噬细胞中使用siRNA沉默Nrf2或在肺泡巨噬细胞中使用Nrf2基因敲除消除了这种效应。此外，rMS使IL-1β和TNF-α炎症基因的表达分别降低了[具体数值未给出]并抑制了p38 MAPK激活。这些发现突出了rMS激活非经典Nrf2途径、调节巨噬细胞功能以及增强宿主对细菌感染防御的能力。
