Streptococcus agalactiae (GBS) is an important pathogen that has increasingly received attention for its role in invasive infections and its broad host range. Research on the regulation of gene expression could illuminate GBS pathogenesis. We previously identified a novel transcriptional regulator XtgS, which is a negative regulator of GBS pathogenicity. Here, we demonstrate that XtgS overexpression significantly attenuated GBS virulence in zebrafish infection tests, and XtgS indirectly downregulated the transcription of two iron transport systems based on the results of transcriptomic analysis, electrophoretic mobility shift assays (EMSAs) and lacZ fusion assays. Subsequent studies verified that the inactivation of iron transport system 1 resulted in GBS excessive iron accumulation and attenuated virulence. Thus, we infer that the downregulation of iron transport system 1 caused by XtgS overexpression probably attenuates bacterial virulence, which partially clarifies the mechanism by which XtgS alleviates the pathogenesis. These findings provide new insights into the relationship between exogenous transcriptional regulation and bacterial virulence.

无乳链球菌(GBS) 是一种重要的病原体，因其在侵袭性感染中的作用及其广泛的宿主范围而越来越受到关注。基因表达调控的研究可以阐明GBS的发病机制。我们以前确定了一种新的转录调节因子 XtgS，它是 GBS 致病性的负调节因子。在这里，我们证明 XtgS 过表达显着减弱了斑马鱼感染测试中 GBS 的毒力，并且根据转录组学分析、电泳迁移率变化分析 (EMSAs) 和lacZ的结果，XtgS 间接下调了两种铁转运系统的转录融合分析。随后的研究证实，铁转运系统 1 的失活导致 GBS 过量铁积累并减弱毒力。因此，我们推断由 XtgS 过表达引起的铁转运系统 1 的下调可能会减弱细菌毒力，这部分阐明了 XtgS 减轻发病机制的机制。这些发现为外源转录调控与细菌毒力之间的关系提供了新的见解。