title: Identification of candidate susceptibility and resistance genes of mice infected with Streptococcus suis type 2.
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.
authors.affiliation: Key Lab of Animal Bacteriology, Ministry of Agriculture, Nanjing Agricultural University, Nanjing, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Rong
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Wang
authors.forename: Hongjie
authors.initials: H
authors.lastname: Fan
authors.forename: Chengping
authors.initials: C
authors.lastname: Lu
authors.forename: Huochun
authors.initials: H
authors.lastname: Yao
mesh_terms: D000818:Animals; D017209:Apoptosis; D060467:Disease Resistance; D015536:Down-Regulation; D020869:Gene Expression Profiling; D020022:Genetic Predisposition to Disease; D007249:Inflammation; D017737:Macrophages, Peritoneal / Q000166:cytology; D051379:Mice; D008810:Mice, Inbred C57BL; D020411:Oligonucleotide Array Sequence Analysis; D010587:Phagocytosis; D060888:Real-Time Polymerase Chain Reaction / Q000379:methods; D015398:Signal Transduction; D013290:Streptococcal Infections / Q000235:genetics / Q000382:microbiology*; D017011:Streptococcus suis / Q000378:metabolism*