A Genome-Wide Survey for Host Response of Silkworm, Bombyx mori during Pathogen Bacillus bombyseptieus Infection

Abstract

Host-pathogen interactions are complex relationships, and a central challenge is to reveal the interactions between pathogens and their hosts. Bacillus bombysepticus (Bb) which can produces spores and parasporal crystals was firstly separated from the corpses of the infected silkworms (Bombyx mori). Bb naturally infects the silkworm can cause an acute fuliginosa septicaemia and kill the silkworm larvae generally within one day in the hot and humid season. Bb pathogen of the silkworm can be used for investigating the host responses after the infection. Gene expression profiling during four time-points of silkworm whole larvae after Bb infection was performed to gain insight into the mechanism of Bb-associated host whole body effect. Genome-wide survey of the host genes demonstrated many genes and pathways modulated after the infection. GO analysis of the induced genes indicated that their functions could be divided into 14 categories. KEGG pathway analysis identified that six types of basal metabolic pathway were regulated, including genetic information processing and transcription, carbohydrate metabolism, amino acid and nitrogen metabolism, nucleotide metabolism, metabolism of cofactors and vitamins, and xenobiotic biodegradation and metabolism. Similar to Bacillus thuringiensis (Bt), Bb can also induce a silkworm poisoning-related response. In this process, genes encoding midgut peritrophic membrane proteins, aminopeptidase N receptors and sodium/calcium exchange protein showed modulation. For the first time, we found that Bb induced a lot of genes involved in juvenile hormone synthesis and metabolism pathway upregulated. Bb also triggered the host immune responses, including cellular immune response and serine protease cascade melanization response. Real time PCR analysis showed that Bb can induce the silkworm systemic immune response, mainly by the Toll pathway. Anti-microorganism peptides (AMPs), including of Attacin, Lebocin, Enbocin, Gloverin and Moricin families, were upregulated at 24 hours post the infection.

Ecdysone Titer Determined by 3DE-3β-Reductase Enhances the Immune Response in the Silkworm

“…This indicated that ecdysone could efficiently influence the immune system of the silkworm. Similar to other insects, silkworm also contains Toll and IMD signaling pathways to stimulate the expressions of different AMP genes, such as cecropin, gloverin, and moricin, although it is still unclear which AMPs are specifically regulated by which pathway (many AMPs can be upregulated by both positive and negative bacteria) (39)(40)(41). To assess the effect of 20E on silkworm innate immunity, we surveyed the transcriptional responses of several immune-related genes, including AMP genes (Gloverin and Morcin), adaptor of the Toll receptor (Myd88), peptidoglycan recognition protein (PGRP-S6), and cellular immune-related gene (C-type lectin).…”

Insect Cytokine Paralytic Peptide (PP) Induces Cellular and Humoral Immune Responses in the Silkworm Bombyx mori

“…Some of those uncharacterized genes induced by active PP share homology with immune-related genes in other insects, like a gene (China gene model ID: BGIBMGA002396, microarray clone ID: Ka06397) that shares homology with the Drosophila spaeztle family (25% identity in the predicted protein sequence), and a gene (BGIBMGA003614, Ka05904) that possesses a tumor necrosis factor (TNF) family signature and showed 27% identity in the predicted protein sequence to eiger, a Drosophila TNF ortholog. (17,18) and B. mori (19), expression of genes encoding phagocytosis-associated proteins (adhesion molecules, cytoskeleton, adaptor molecules, etc. ), AMPs, and pattern recognition receptors are up-regulated by infectious stimuli.…”

Midgut immune responses induced by bacterial infection in the silkworm, Bombyx mori

“…B. bombysepticus, which produces spores and parasporal crystals, was reported to be a highly pathogenic bacterium in silkworms. B. bombysepticus oral infection could provoke strong host immune responses (Huang et al, 2009). In our study, we rarely found live P. aeruginosa in the gut at 12 h after oral infection (Fig.…”