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<i>E. coli</i> is a ubiquitous pathogen that is responsible for over one million fatalities worldwide on an annual basis. In animals, <i>E. coli</i> can cause a variety of diseases, including mastitis in dairy cattle, which represents a potential public health hazard. However, the pathophysiology of <i>E. coli</i> remains unclear. We found that <i>E. coli</i> could induce global upregulation of m⁶A methylation and cause serious apoptosis in bovine mammary epithelial cells (MAC-T cells). Furthermore, numerous m⁶A-modified lncRNAs were identified through MeRIP-seq. Interestingly, we found that the expression of LOC4191 with hypomethylation increased in MAC-T cells upon <i>E. coli</i>-induced apoptosis. Knocking down LOC4191 promoted <i>E. coli</i>-induced apoptosis and ROS levels through the caspase 3–PARP pathway. Meanwhile, knocking down ALKBH5 resulted in the promotion of apoptosis through upregulated ROS and arrested the cell cycle in MAC-T cells. ALKBH5 silencing accelerated LOC4191 decay by upregulating its m⁶A modification level, and the process was recognized by hnRNP A1. Therefore, this indicates that ALKBH5 stabilizes m⁶A-modified LOC4191 to suppress <i>E. coli</i>-induced apoptosis. This report discusses an initial investigation into the mechanism of m⁶A-modified lncRNA in cells under <i>E. coli</i>-induced apoptosis and provides novel insights into infectious diseases.