Steap3 is a key node in regulating the phagosome escape of Listeria monocytogenes

Listeria monocytogenes, a foodborne pathogen, poses a significant threat to human health due to its high mortality rate and increasing antibiotic resistance. This study investigates the role of Steap3 in regulating the early phagosomal escape of Listeria monocytogenes. We found that Steap3 expression is downregulated in dendritic and intestinal epithelial cells following infection, and its deficiency exacerbates bacterial proliferation both in vitro and in vivo. Mechanistically, Steap3 interacts with Gm2a and Sting to inhibit Listeria monocytogenes infection. Our results highlight Steap3 as a key regulator in dendritic and intestinal epithelial cells' defense against Listeria monocytogenes infection, suggesting the Steap3-STING/Gm2a axis is a potential therapeutic target for listeriosis. This study provides valuable insights into the molecular mechanisms underlying Listeria monocytogenes pathogenesis and host immune response, offering new directions for developing anti-Listeria monocytogenes therapies.