<b>SPD_0410 负调控胶囊多糖的合成和毒力</b><b><i>肺炎链球菌</i></b><b> D39</b>

<i> </i><i>Streptococcus pneumoniae </i>capsular polysaccharide (CPS) is a crucial virulence factor for this pathogenic bacterium and is partially under transcriptional control. In this study, weused electrophoretic mobility shift assaysand DNA enzyme footprintingto identified the hypothetical protein SPD_0410 as a negative regulator of cps locus. Our results showed that the D39Δ<i>spd0410</i> mutant strain exhibited significantly elevated CPS levels compared to the parental strain D39s. SPD_0410 directly binds at two specific sites on the cps promoter. The regulatory effect of SPD_0410 on CPS was weakened after the mutation of specific binding sites in the promoter.RNAseq analysis revealed that the deletion of <i>spd0410</i> led to alterations in glucose metabolism. However, the altered glucose levels appeared to eliminate the regulation of CPS synthesis by SPD_0410. Deleting the <i>spd0410</i> gene resulted in higher invasion and phagocytic resistance of bacteria and in vivo mouse experiments confirmed that D39Δ<i>spd</i><i>0410</i><i> </i>caused more severe systemic disease than the parental strain D39s. Our results indicated that SPD_0410 negatively regulates the synthesis of <i>S. pneumoniae</i> capsules and can directly alter pneumococcal virulence.