Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Biomed Pharmacother. 2024 Sep;178:117193. doi: 10.1016/j.biopha.2024.117193. Epub 2024 Jul 26.
Mycobacterium bovis (M. bovis) Bacillus Calmette-Guerin (BCG) strain used in immunotherapy of bladder cancer (onco-BCG) due to its acid tolerance can be a candidate for prevention or reversion of deleterious effects towards gastric cell barrier initiated by gastric pathogen Helicobacter pylori (Hp) with high resistance to commonly used antibiotics. Colonization of gastric mucosa by Hp promotes oxidative stress, apoptosis resulting in the gastric barrier damage. The aim of this study was to examine the ability of onco-BCG bacilli to control the Hp driven gastric damage using the model of Cavia porcellus primary gastric epithelial cells or fibroblasts in vitro. These cells were treated with Hp surface antigens (glycine acid extract-GE or lipopolysaccharide-LPS) alone or with onco-BCG bacilli and evaluated for cell apoptosis and proliferation in conjunction with the level of soluble lipid peroxidation marker (s4HNE). The cell migration was determined by "wound healing assay", while cytokine response of cells, including interleukin (IL)-33, IL-1β, IL-8 and tumor necrosis factor alpha (TNF-α), by the ELISA. The apoptosis of cells pulsed in vitro with Hp surface components present in GE or with LPS was reduced after exposure of cells to mycobacteria. Similarly, the cell regeneration which was diminished by Hp LPS has been improved in response to mycobacteria. This study reveals that vaccine mycobacteria may reduce gastric barrier damage induced by Hp infection.
牛分枝杆菌（M. bovis）卡介苗（BCG）菌株用于膀胱癌的免疫治疗（肿瘤卡介苗），由于其耐酸性，可以成为预防或逆转幽门螺杆菌（Hp）引起的胃细胞屏障损伤的候选物，而 Hp 对常用抗生素具有高度耐药性。Hp 对胃黏膜的定植会促进氧化应激，导致细胞凋亡，从而导致胃屏障损伤。本研究旨在使用体外原代胃上皮细胞或成纤维细胞的 Cavia porcellus 模型，研究肿瘤卡介苗杆菌控制 Hp 驱动的胃损伤的能力。这些细胞单独用 Hp 表面抗原（甘氨酸酸提取物-GE 或脂多糖-LPS）或用肿瘤卡介苗杆菌处理，并结合可溶性脂质过氧化标记物（s4HNE）的水平评估细胞凋亡和增殖。细胞迁移通过“划痕愈合试验”确定，细胞因子反应，包括白细胞介素（IL）-33、IL-1β、IL-8 和肿瘤坏死因子-α（TNF-α），通过 ELISA 确定。暴露于分枝杆菌后，体外脉冲 Hp 表面成分（存在于 GE 或 LPS 中）的细胞凋亡减少。同样，Hp LPS 减弱的细胞再生在分枝杆菌的作用下得到了改善。这项研究表明，疫苗分枝杆菌可能减少 Hp 感染引起的胃屏障损伤。
