Streptococcus salivarius inhibits immune activation by periodontal disease pathogens

Kyle W MacDonald; Ryan M Chanyi; Jean M Macklaim; Peter A Cadieux; Gregor Reid; Jeremy P Burton

doi:10.1186/s12903-021-01606-z

Streptococcus salivarius inhibits immune activation by periodontal disease pathogens

BMC Oral Health. 2021 May 7;21(1):245. doi: 10.1186/s12903-021-01606-z.

Authors

Kyle W MacDonald^{1

2}, Ryan M Chanyi^{1

2}, Jean M Macklaim^{2

3}, Peter A Cadieux^{2

4}, Gregor Reid^{1

2}, Jeremy P Burton^{5

6

7}

Affiliations

¹ Department of Microbiology and Immunology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
² Canadian Centre for Human Microbiome and Probiotic Research, Lawson Health Research Institute, London, ON, Canada.
³ Department of Biochemistry, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
⁴ School of Health Sciences, Fanshawe College, London, ON, Canada.
⁵ Department of Microbiology and Immunology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada. jeremy.burton@lawsonresearch.com.
⁶ Canadian Centre for Human Microbiome and Probiotic Research, Lawson Health Research Institute, London, ON, Canada. jeremy.burton@lawsonresearch.com.
⁷ Department of Surgery, Division of Urology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada. jeremy.burton@lawsonresearch.com.

Abstract

Background: Periodontal disease represents a major health concern. The administration of beneficial microbes has been increasing in popularity over efforts to manipulate the microbes using antimicrobial agents. This study determined the ability of Streptococcus salivarius to inhibit IL-6 and IL-8 production by gingival fibroblasts when activated by periodontal pathogens and their effect on the salivary microbiome.

Methods: Primary human gingival fibroblasts were challenged with Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans and Fusobacterium nucleatum and a combination of all three. IL-6 and IL-8 cytokine release were measured. Using this same model, S. salivarius K12, M18 and different supernatant and whole-cell lysate fractions of S. salivarius K12 were administered to pathogen-induced fibroblasts. A patient study of healthy participants was also conducted to determine the effect S. salivarius K12 had on the native microbiome using 16S next generation sequence analysis.

Results: All pathogens tested induced a significant IL-6 and IL-8 response. S. salivarius K12 or M18, did not exhibit an increase in inflammatory cytokines. When either of the probiotic strains were co-administered with a pathogen, there were significant reductions in both IL-6 and IL-8 release. This effect was also observed when gingival fibroblasts were pre-treated with either S. salivarius K12 or M18 and then stimulated with the oral pathogens. Chewing gum containing S. salivarius K12 did not alter the salivary microbiome and did not increase inflammatory markers in the oral cavity.

Conclusion: S. salivarius K12 and M18 prevented immune activation induced by periodontal disease pathogens. S. salivarius K12 did not alter the salivary microbiome or induce immune activation when administered as a chewing gum. These results warrant further study to determine if it may be an effective treatment in a model of periodontal disease.

Keywords: Aggregatibacter actinomycetemcomitans; Chewing gum; Fusobacterium nucleatum; Immune inhibition; Periodontal disease; Porphyromonas gingivalis; Probiotics; Streptococcus salivarius.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Aggregatibacter actinomycetemcomitans
Fusobacterium nucleatum
Humans
Periodontal Diseases*
Porphyromonas gingivalis
Streptococcus salivarius*