Comparative transcriptomic analysis reveal genes involved in the pathogenicity increase of Streptococcus suis epidemic strains. Issue 1 (31st December 2022)

• Record Type: Journal Article
• Authors: Wang, Jianping; Liang, Pujun; Sun, Hui; Wu, Zongfu; Gottschalk, Marcelo; Qi, Kexin; Zheng, Han
• Is Part Of: Virulence. Volume 13:Issue 1(2022)
• Page Start: 1455
• Page End: 1470
• Publication Date: 2022-12-31
• Subjects: Streptococcus suis -- epidemic strains -- pathogenicity increase -- comparative transcriptome -- methionine -- surface proteins; Virulence (Microbiology) -- Periodicals; Bacterial diseases -- Periodicals; Molecular microbiology -- Periodicals; 579.05
• DOI: 10.1080/21505594.2022.2116160
• Languages: English
• ISSNs: 2150-5608

Abstract

ABSTRACT: Streptococcus suis epidemic strains were responsible for two outbreaks in China and possessed increased pathogenicity which was featured prominently by inducing an excessive inflammatory response at the early phase of infection. To discover the critical genes responsible for the pathogenicity increase of S. suis epidemic strains, the genome-wide transcriptional profiles of epidemic strain SC84 were investigated at the early phase of interaction with BV2 cells. The overall low expression levels of 89K pathogenicity island (PAI) and 129 known virulence genes in the SC84 interaction groups indicated that its pathogenicity increase should be attributed to novel mechanisms. Using highly pathogenic strain P1/7 and intermediately pathogenic strain 89–1591 as controls, 11 pathogenicity increase crucial genes (PICGs) and 38 pathogenicity increase-related genes (PIRGs) were identified in the SC84 incubation groups. The PICGs encoded proteins related to the methionine biosynthesis/uptake pathway and played critical roles in the pathogenicity increase of epidemic strains. A high proportion of PIRGs encoded surface proteins related to host cell adherence and immune escape, which may be conducive to the pathogenicity increase of epidemic strains by rapidly initiating infection. The fact that none of PICGs and PIRGs belonged to epidemic strain-specific gene indicated that the pathogenicity increase of epidemic strain may be determined by the expression level of genes, rather than the presence of them. Our results deepened the understanding on the mechanism of the pathogenicity increase of S. suis epidemic strains and provided novel approaches to control the life-threatening infections of S. suis epidemic strains.