BACKGROUNDAsian citrus psyllid, Diaphorina citri, is a notorious pest in citrus industry because it transmits Candidatus Liberibacter asiaticus, which causes an uncurable, devastating disease in citrus worldwide. Serratia marcescens is widely distributed in various environments that exhibits toxic effects to many insects. To develop strategies for enhancing the efficiency of pathogen‐induced host mortality, a better understanding of the toxicity mechanism of S. marcescens on D. citri is critical.RESULTSS. marcescens KH‐001 successfully colonized D. citri gut by feeding artificial diets, resulting in the damage of cells including nucleus, mitochondria, vesicles, and microvilli. Oral ingestion of S. marcescens KH‐001 strongly induced apoptosis in gut cells by enhancing levels of Cyt c, p53 and caspase‐1 and decreasing levels of inhibitors of apoptosis (IAP) and Bax inhibitor‐1 (BI‐1). The expression of dual oxidase (Duox) and nitric oxide synthase (Nos) was up‐regulated by S. marcescens KH‐001, which increased hydrogen peroxide (H2O2) levels in the gut. Injection of abdomen of D. citri with H2O2 accelerated the death of the adults and induced apoptosis in the gut cells by activating Cyt c, p53 and caspase‐1 and suppressing IAP and BI‐1. Pretreatment of infected D. citri with vitamin c (Vc) increased the adult survival and diminished the apoptosis‐inducing effect.CONCLUSIONSThe colonization of S. marcescens KH‐001 in the guts of D. citri increased H2O2 accumulation, leading to severe changes and apoptosis in intestinal cells, which enhanced a higher mortality level of D. citr. This study identifies the underlying virulence mechanism of S. marcescens KH‐001 on D. citri that contributes to a widespread application in the integrated management of citrus psyllid.This article is protected by copyright. All rights reserved.