Serratia marcescens SM001-induced oxidative stress accelerates Spodoptera frugiperda mortality by promoting midgut apoptosis.

Abstract

Spodoptera frugiperda (fall armyworm) is a globally distributed and highly destructive migratory pest, while Serratia marcescens is a widespread entomopathogenic bacterium capable of infecting diverse insects. In this study, oral infection with S. marcescens strain SM001 exhibited potent virulence, with an LC50 of 7.40 × 106 CFU/mL at 168 h post-infection (hpi). Logistic regression modeling demonstrated that the bacterium enters an exponential proliferation phase within the hemolymph approximately 48-54 h after infection. Infection significantly upregulated Duox and Nos, induced severe oxidative stress, and activated an apoptotic cascade involving Cyt c, p53, and caspase, culminating in extensive midgut epithelial cell apoptosis. Mitigating oxidative stress via targeted Vitamin C supplementation or Duox knockdown alleviated midgut tissue damage and delayed bacterial dissemination. However, exogenous Vitamin C treatment decreased larval mortality, whereas Duox knockdown failed to improve overall survival, revealing a critical physiological trade-off between ROS-mediated pathogen clearance and host immunopathology. Overall, SM001 disrupts midgut redox homeostasis, drives excessive H2O2 accumulation, and breaches the intestinal barrier to facilitate hemocoel translocation, ultimately leading to lethal systemic septicemia. These findings highlight the pivotal role of host-mediated immunopathology in bacterial pathogenesis and provide a robust theoretical foundation for developing advanced microbial control strategies against S. frugiperda.