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Research Paper

The antimicrobial systems of Streptococcus suis promote niche competition in pig tonsils

ORCID Icon, , , , , , , ORCID Icon, & ORCID Icon show all
Pages 781-793 | Received 22 Dec 2021, Accepted 18 Apr 2022, Published online: 28 Apr 2022
 

ABSTRACT

Streptococcus suis can cause severe infections in pigs and humans. The tonsils of pigs are major niches for S. suis, and different serotypes of S. suis can be found in the same tonsil. Pig tonsil colonization by S. suis is believed to be an important source of infection for humans and pigs. However, how S. suis competes for a stable tonsil niche is unknown. Here, we found that S. suis strain WUSS351, isolated from a healthy pig tonsil, is virulent and multidrug-resistant. The ABC transporter system SstFEG, conferring resistance to bacitracin, was reported to confer a competitive survival advantage in vivo. In addition, strain WUSS351 has several antimicrobial systems, including a novel type VII secretion system (T7SS), lantibiotic bacteriocin, and lactococcin972-like bacteriocin Lcn351. Bacterial competition experiments demonstrated T7SS-mediated cell contact-dependent antagonism of S. suis. Antibacterial activity analysis and 16S rRNA gene sequencing of the culture-independent and culture-dependent pig tonsillar microbiome revealed that Lcn351 mainly targets S. suis, one of the core microbiomes in pig tonsils. Taken together, our results revealed the mechanism of the stable persistence of S. suis in the tonsil niche, which might have important implications for S. suis epidemiology, potentially influencing strain prevalence and disease progression.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The complete genome sequence of strain WUSS351 was deposited in GenBank and received the accession number NZ_CP039462.1. The data supporting this study’s findings are available from the corresponding author upon reasonable request.

Supplementary material

Supplemental data for this article can be accessed here

Additional information

Funding

The work was supported by the National Key Research and Development Program of China [2021YFD1800402]; National Natural Science Foundation of China [32172859]; National Natural Science Foundation of China [31872469]; Open Project Program of Jiangsu Key Laboratory of Zoonosis [R2103]; Open Project Program of Engineering Research Center for the Prevention and Control of Animal Original Zoonosis, Fujian Province University [2021ZW001].