Hong Yaming, Hou Qilong, Liu Hui, Wang Xiaojie, Gu Jiaojie, Wang Zhenyu, Jiao Xinan, Li Qiuchun
Jiangsu Key Lab of Zoonosis/Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou, China.
Key Laboratory of Prevention and Control of Biological Hazard Factors (Animal Origin) for Agri-Food Safety and Quality, Ministry of Agriculture of China, Yangzhou University, Yangzhou, China.
Vet Res. 2024 Dec 18;55(1):166. doi: 10.1186/s13567-024-01427-2.
Over the past two decades, the monophasic variant of Salmonella enterica serovar Typhimurium (S. Typhimurium) has rapidly emerged and increased worldwide. This upsurge is especially true for the European clone of the ST34 S. Typhimurium monophasic variant. The key distinction between ST34 S. Typhimurium and its monophasic variant is that the genes that encode for second-phase flagellin (FljB) and the regions around it have been replaced with various multidrug resistance cassettes. To determine if the loss of fljB or the retention of fliC,-the gene coding for first-phase flagellin (FliC)-, would impact its pathogenicity, we constructed various mutations, including deletions of fljB, fliC, fliC/fljB, and strains where fliC was replaced with fljB. Our results showed that the loss of fljB in ST34 S. Typhimurium and its monophasic variant does not affect bacterial motility, cell infection ability, survival in macrophages, induced pro-inflammatory cytokines secretion, virulence, or persistent infection in mice. However, the deletion of fliC caused a significant decrease in these outcomes for both strains, while the replacement of fliC with fljB only partially restored these capabilities. Consequently, we determined that FliC is predominant in the flagellar expression of ST34 S. Typhimurium other than FljB. This finding demonstrates that replacing the fljB gene with various resistance regions in ST34 S. Typhimurium monophasic variants can enhance bacterial survival under specific antibiotic farming practices and spread globally.
在过去二十年中，肠炎沙门氏菌鼠伤寒血清型（鼠伤寒沙门氏菌）的单相变体在全球范围内迅速出现并增加。这种激增在ST34鼠伤寒沙门氏菌单相变体的欧洲克隆中尤为明显。ST34鼠伤寒沙门氏菌与其单相变体之间的关键区别在于，编码第二阶段鞭毛蛋白（FljB）及其周围区域的基因已被各种多药耐药盒所取代。为了确定fljB的缺失或第一阶段鞭毛蛋白（FliC）编码基因fliC的保留是否会影响其致病性，我们构建了各种突变体，包括fljB、fliC、fliC/fljB的缺失，以及fliC被fljB取代的菌株。我们的结果表明，ST34鼠伤寒沙门氏菌及其单相变体中fljB的缺失不影响细菌的运动性、细胞感染能力、在巨噬细胞中的存活、诱导促炎细胞因子的分泌、毒力或在小鼠中的持续感染。然而，fliC的缺失导致这两种菌株的这些结果显著下降，而用fljB取代fliC仅部分恢复了这些能力。因此，我们确定在ST34鼠伤寒沙门氏菌的鞭毛表达中，FliC比FljB更占主导地位。这一发现表明，在ST34鼠伤寒沙门氏菌单相变体中用各种抗性区域取代fljB基因可以增强细菌在特定抗生素养殖实践下的生存能力并在全球传播。
