Groupe de Recherche sur les Maladies Infectieuses du Porc and Centre de Recherche en Infectiologie Porcine, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, Canada.
PLoS One. 2010 Jan 5;5(1):e8426. doi: 10.1371/journal.pone.0008426.
Pili have been shown to contribute to the virulence of different Gram-positive pathogenic species. Among other critical steps of bacterial pathogenesis, these structures participate in adherence to host cells, colonization and systemic virulence. Recently, the presence of at least four discrete gene clusters encoding putative pili has been revealed in the major swine pathogen and emerging zoonotic agent Streptococcus suis. However, pili production by this species has not yet been demonstrated. In this study, we investigated the functionality of one of these pili clusters, known as the srtF pilus cluster, by the construction of mutant strains for each of the four genes of the cluster as well as by the generation of antibodies against the putative pilin subunits. Results revealed that the S. suis serotype 2 strain P1/7, as well as several other highly virulent invasive S. suis serotype 2 isolates express pili from this cluster. However, in most cases tested, and as a result of nonsense mutations at the 5' end of the gene encoding the minor pilin subunit (a putative adhesin), pili were formed by the major pilin subunit only. We then evaluated the role these pili play in S. suis virulence. Abolishment of the expression of srtF cluster-encoded pili did not result in impaired interactions of S. suis with porcine brain microvascular endothelial cells. Furthermore, non-piliated mutants were as virulent as the wild type strain when evaluated in a murine model of S. suis sepsis. Our results show that srtF cluster-encoded, S. suis pili are atypical compared to other Gram-positive pili. In addition, since the highly virulent strains under investigation are unlikely to produce other pili, our results suggest that pili might be dispensable for critical steps of the S. suis pathogenesis of infection.
菌毛有助于不同革兰氏阳性致病菌的毒力。在细菌发病机制的其他关键步骤中,这些结构参与与宿主细胞的黏附、定植和全身毒力。最近,在主要的猪病原体和新兴的人畜共患病原猪链球菌中,至少发现了四个不同的基因簇,这些基因簇编码推测的菌毛。然而,该物种的菌毛产生尚未得到证实。在这项研究中,我们通过构建该基因簇的四个基因的突变株以及针对推测的菌毛亚基产生抗体,研究了该基因簇之一,即 srtF 菌毛簇的功能。结果表明,猪链球菌血清型 2 株 P1/7 以及其他几种高毒力侵袭性猪链球菌血清型 2 分离株表达来自该簇的菌毛。然而,在大多数测试的情况下,由于编码次要菌毛亚基(一种推测的黏附素)的基因 5' 端的无意义突变,只有主要菌毛亚基形成菌毛。然后,我们评估了这些菌毛在猪链球菌毒力中的作用。srtF 簇编码菌毛的表达缺失不会导致猪链球菌与猪脑微血管内皮细胞的相互作用受损。此外,在猪链球菌败血症的小鼠模型中评估时,无菌毛突变体与野生型菌株一样具有毒力。我们的结果表明,srtF 簇编码的猪链球菌菌毛与其他革兰氏阳性菌毛不同。此外,由于研究中高度毒力的菌株不太可能产生其他菌毛,我们的结果表明菌毛可能对猪链球菌感染发病机制的关键步骤是可有可无的。