https://orcid.org/0000-0001-6882-7520
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ABSTRACT
Streptococcus suis
serotype 2 (S. suis 2) is an important swine pathogen and also an emerging zoonotic agent. HtpsA has been reported as an immunogenic cell surface protein on the bacterium. In the present study, we constructed an isogenic mutant strain of htpsA, namely ΔhtpsA, to study its role in the development and virulence of S. suis 2. Our results showed that the mutant strain lost its typical encapsulated structure with decreased concentrations of sialic acid. Furthermore, the survival rate in whole blood, the anti-phagocytosis by RAW264.7 murine macrophage, and the adherence ability to HEp-2 cells were all significantly affected in the ΔhtpsA. In addition, the deletion of htpsA sharply attenuated the virulence of S. suis 2 in an infection model of mouse. RNA-seq analysis revealed that 126 genes were differentially expressed between the ΔhtpsA and the wild-type strains, including 28 upregulated and 98 downregulated genes. Among the downregulated genes, many were involved in carbohydrate metabolism and synthesis of virulence-associated factors. Taken together, htpsA was demonstrated to play a role in the morphological development and pathogenesis of the highly virulent S. suis 2 05ZYH33 strain.
Acknowledgments
We thank Dr. Daisuke Takamatsu at the National Institute of Animal Health of Japan for the generous gifts of the E. coli-S. suis shuttle vectors pSET2. We thank LetPub (www.letpub.com) for its linguistic assistance during the preparation of this manuscript. The raw sequencing data were submitted to NCBI’s Gene Expression Omnibus (accession number PRJNA644160).
Disclosure statement
No potential conflict of interest was reported by the authors.
Supplemental data
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