DnaJ of Streptococcus suis Type 2 Contributes to Cell Adhesion and Thermotolerance

Abstract

To examine if the molecular chaperone DnaK operon proteins of Streptococcus suis type 2 (SS2) are involved in adhesion to host cells, the abundance values of these proteins from the surface of two SS2 strains of different adhesion capability were compared. Their roles in growth and adhesion to human laryngeal epithelial cell line HEp-2 cells were investigated on SS2 strain HA9801 and its mutants with DnaK operon genes partially knocked-out (PKO mutant) under heat stress. The major difference was that DnaJ was more abundant in strain HA9801 than in strain JX0811. Pretreatment of the bacteria with hyperimmune sera to DnaJ, but not with those to other proteins, could significantly reduce SS2 adhesion to HEp-2 cells. PKO of dnaJ g ene resulted in decreased SS2 growth at 37 °C and 42 °C, and reduced its adhesion to HEp-2 cells. The wild-type strain stressed at 42 °C had increased expression of DnaJ on its surface and elevated adhesion to HEp-2 cells, which was also inhibitable by DnaJ specific antiserum. These results indicate that the DnaJ of S. suis type 2 is important not only for thermotolerance but also for adhesion to host cells. Because DnaJ expression is increased upon temperature upshift with increased exposure on the bacterial surface, the febrile conditions of the cases with systemic infections might help facilitate bacterial adhesion to host cells. DnaJ could be one of the potential candidates as a subunit vaccine because of its good immunogenicity.

Identification of conditionally essential genes for Streptococcus suis infection in pigs

“…Certainly, several mutants that participated in stress responses (grpE, dnaK, tig) were attenuated for growth at diverse sites of infection (Table 1). The gene encoding the chaperone DnaJ of S. suis was shown to contribute to thermotolerance [56], whereas in S. pneumoniae, DnaJ was shown to play an important role in inflammatory responses [57]. Trigger factor, another chaperone with peptidyl-prolyl cis-trans isomerization that assists proteins in its proper folding and maturation [58], was shown to contribute to stress tolerance and alter the expression of genes involved in virulence in S. suis [59] and other pathogenic streptococci [60].…”

“…Trigger factor, another chaperone with peptidyl-prolyl cis-trans isomerization that assists proteins in its proper folding and maturation [58], was shown to contribute to stress tolerance and alter the expression of genes involved in virulence in S. suis [59] and other pathogenic streptococci [60]. Besides assisting in stress responses, a role in adhesion was attributed to these proteins [56,60], although adhesion mediated by these cytoplasmic chaperones remains controversial. Even when they lack a signal peptide required for secretion and a cell wall anchor motif, they were partially found at the cell surface [60].…”

“…stabilization likely imported by the cited transporters [75]. Other chaperones such as DnaJ, which possess a demonstrated function in thermotolerance of S. suis serotype 2 [56], needs Zinc for the recognition of substrates [76]. In contrast to the cited mutants, mutant 10ΔglA lacked a depressed logarithmic phase as observed for the wild type (Figure 4(b)).…”

Ribose operon repressor (RbsR) contributes to the adhesion of Aeromonas hydrophila to Anguilla japonica mucus

“…Experiments with the pathogens Pseudomonas aeruginosa , Vibrio alginolyticus; Vibrio vulnificus, and Legionella pneumophila (Huang, Hu et al., ; Kim & Rhee, ; Luo et al., ; Olga, Jens, & Michael, ; Shao et al., ) demonstrated the important role of flagella or lipopoly saccharides in establishing the initial interaction with mucosal surfaces or cells and that this defect can reduce the ability of adhesion. In addition, the genetic basis of colonization has been studied in V. vulnificus , L. pneumophila, and Streptococcus suis (Chang et al., ; Kim & Rhee, ; Zhang et al., ) and in the genes that impact bacterial adhesion that can also contribute to bacterial pathogenesis. In the pathogenic bacteria V. vulnificus , FlgC was shown to be involved in adhesion to HeLa cells, and the flgC mutation could decrease the level of adhesion, cytotoxicity, and lethality in mice (Kim & Rhee, ).…”

“…Intracellular bacteria L. pneumophilalaia was shown to be involved in adhesion to the human lung alveolar epithelial cell line A549, and the laiA gene mutation could cause reduced mortality in A/J mice (Chang et al., ). The dnaJ of S. suis Type 2 was important for adhesion to host cells, and the dnaJ PKO strain can result in reduced adhesion to cultured cell monolayers (Zhang et al., ). These pathogenic genes were all considered to be the key factors for bacterial adhesion and pathogenicity.…”