Activation of the Host Immune Response in Hyphantria cunea (Drury) (Lepidoptera: Noctuidae) Induced by Serratia marcescens Bizio.

Abstract

Simple SummaryHyphantria cunea (Drury) is a quarantine pest, due to its extensive host, leading to serious economic losses in the agricultural and forestry industries. To control this pest, it is increasingly important to use microbial pesticides because they are biologically active and ecologically safe. Serratia marcescens Bizio (SM1) is a potential biocontrol bacterium. Although SM1 has a pathogenic role in H. cunea, H. cunea self-defense reduces the pathogenic effect of SM1. In this study, immune-related differentially expressed genes (DEGs) in H. cunea were first identified after SM1 infection, and the immune regulation mode of H. cunea in response to SM1, including antimicrobial peptide synthesis pathways, melanization and cellular immunity, was revealed. According to the analysis, the immune system of H. cunea was induced by SM1. In summary, our study demonstrates how the immune systems of the H. cunea work to resist the infection of SM1, which provides the theoretical basis for researching more efficient microbial pesticides for H. cunea.Host–pathogen interactions are essential to our understanding of biological pesticides. Hyphantria cunea (Drury) is an important forest pest worldwide. The immune mechanism of the interaction between H. cunea and Serratia marcescens Bizio (SM1) is unclear. First, transcriptome sequencing and quantitative real-time PCR (qRT-PCR) analysis described the H. cunea immune response to SM1. A total of 234 immune-related differentially expressed genes (DEGs) were found. Many immune regulatory genes in three classical pathways were found. Antimicrobial peptides, including attacin B, cecropin A, gloverin, lebocin and diapausin, are involved in defending against SM1 challenge, and are mainly produced by Toll and immune deficiency (IMD) pathways. Some melanization genes were changed in H. cunea, which suggested that H. cunea melanization was activated by SM1. Furthermore, phagocytosis, autophagolysosome and apoptosis pathways in cellular immunity were activated in H. cunea against SM1. Finally, the expression patterns of 10 immune genes were analyzed systematically by qRT-PCR, and most of the genes were upregulated compared to the control. Our studies provide useful information about the immune response of H. cunea under the stress of SM1, which is important to understand how SM1 affects the immune system of H. cunea and provides new ideas to control H. cunea by using SM1.