Heat-killed Lactobacillus acidophilus mediates Fusobacterium nucleatum induced pro-inflammatory responses in epithelial cells

• Published in: FEMS microbiology letters Vol. 368; no. 5; pp. 1 - 8
• Main Authors: Ding, Qinfeng, Sun, Xuecheng, Cao, Shuai, Zhao, Cancan, Wang, Yitong, Wang, Xudong
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 01.03.2021
• Subjects: Analysis; Bacteria; Biofilms; Cell adhesion; Cytokines; Epithelial cells; Epithelium; Fusobacterium nucleatum; Gene expression; Gram-negative bacteria; Gum disease; Heat; Inflammation; Lactobacilli; Lactobacillus acidophilus; Microbiology; Pathogenesis; Pathogens; Periodontal disease; Periodontal diseases; Probiotics; Virulence; Virulence (Microbiology); China; inflammatory response; coaggregation; periodontal disease; heat-killed probiotics; L. acidophilus
• ISSN: 1574-6968; 0378-1097; 1574-6968
• DOI: 10.1093/femsle/fnaa160

Abstract Probiotics is widespreadly used nowadays. However, the safety issue with the use of live probiotics is still a matter of contention. In recent years, an expanding body of evidence supports the beneficial role of heat-killed probiotics in the maintenance of systemic health, whereas the role of these heat-killed bacteria on periodontal health remains unclear. This study aimed to evaluate the effects of heat-killed probiotics on periodontal pathogen virulence and associated mechanisms. We demonstrated that heat-killed Lactobacillus acidophilus was able to coaggregate with Fusobacterium nucleatum, the bridging bacteria of oral biofilm, and inhibit the adhesion and invasion of F. nucleatum, leading to a subsequent elimination of pro-inflammatory cytokine production in oral epithelial cells. This coaggregation further caused a suppression of the virulence gene fap2 expression in F. nucleatum. Therefore, heat-killed L. acidophilus might downregulate the pro-inflammatory cytokine expression in epithelial cells via coaggregation with F. nucleatum and suppression of F. nucleatum fap2 expression, which was the first demonstration that heat-killed probiotics modulate periodontal disease pathogenesis via coaggregation. Collectively, this finding provides new evidence that heat-killed probiotics might exert beneficial effects to periodontal health by coaggregating with periodontal pathogens and modulating their virulence. Heat-killed Lactobacillu acidophilus might exert beneficial effects to periodontal health by coaggregating with Fusobacterium nucleatum, the bridging pathogens of plaque biofilm and modulating its virulence.