Abstract
Streptococcus suis type 2 (SS2) is an important swine pathogen and zoonosis agent. A/J mice are significantly more susceptible than C57BL/6 (B6) mice to SS2 infection, but the genetic basis is largely unknown. Here, alterations in gene expression in SS2 (strain HA9801)-infected mice were identified using Illumina mouse BeadChips. Microarray analysis revealed 3,692 genes differentially expressed in peritoneal macrophages between A/J and B6 mice due to SS2 infection. Between SS2-infected A/J and control A/J mice, 2646 genes were differentially expressed (1469 upregulated; 1177 downregulated). Between SS2-infected B6 and control B6 mice, 1449 genes were differentially expressed (778 upregulated; 671 downregulated). These genes were analyzed for significant Gene Ontology (GO) categories and signaling pathways using the Kyoto Encylopedia of Genes and Genomes (KEGG) database to generate a signaling network. Upregulated genes in A/J and B6 mice were related to response to bacteria, immune response, positive regulation of B cell receptor signaling pathway, type I interferon biosynthesis, defense and inflammatory responses. Additionally, upregulated genes in SS2-infected B6 mice were involved in antigen processing and presentation of exogenous peptides, peptide antigen stabilization, lymphocyte differentiation regulation, positive regulation of monocyte differentiation, antigen receptor-mediated signaling pathway and positive regulation of phagocytosis. Downregulated genes in SS2-infected B6 mice played roles in glycolysis, carbohydrate metabolic process, amino acid metabolism, behavior and muscle regulation. Microarray results were verified by quantitative real-time PCR (qRT-PCR) of 14 representative deregulated genes. Four genes differentially expressed between SS2-infected A/J and B6 mice, toll-like receptor 2 (Tlr2), tumor necrosis factor (Tnf), matrix metalloproteinase 9 (Mmp9) and pentraxin 3 (Ptx3), were previously implicated in the response to S. suis infection. This study identified candidate genes that may influence susceptibility or resistance to SS2 infection in A/J and B6 mice, providing further validation of these models and contributing to understanding of S. suis pathogenic mechanisms.
Highlights
Streptococcus suis, a Gram-positive encapsulated coccus, is considered to be an important swine pathogen, which causes septicemia and affects the central nervous system (CNS) and other tissues, leading to meningitis, endocarditis, pneumonia and arthritis [1,2]
Bacteria were grown overnight on sheep blood agar plates at 37uC, and isolated colonies were inoculated into 5 mL cultures of Todd-Hewitt broth (THB) (Oxoid), which were incubated for 12 h at 37uC with agitation
The LD50 of strain HA9801 was determined by injecting mice with various doses, and mortality was monitored until 7 days post
Summary
Streptococcus suis, a Gram-positive encapsulated coccus, is considered to be an important swine pathogen, which causes septicemia and affects the central nervous system (CNS) and other tissues, leading to meningitis, endocarditis, pneumonia and arthritis [1,2]. S. suis does cause disease in pigs and affects humans. Human infection with S. suis mainly occur in people with occupational exposure to infected pigs or raw pork products and have been reported in different Asian and European countries, as well as in New Zealand, Australia, Argentina and Canada [4,5,6,7]. The pathogenesis of both systemic and CNS infections caused by S. sius is poorly understood. The route of infection is mainly through skin injuries when bacteria may gain access to the bloodstream, where they disseminate freely or as cellbound bacteria attached to phagocytes [2] until reaching the CNS
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