A concerted probiotic activity to inhibit periodontitis-associated bacteria

Abstract

Periodontitis can result in tooth loss and the associated chronic inflammation can provoke several severe systemic health risks. Adjunctive to mechanical treatment of periodontitis and as alternatives to antibiotics, the use of probiotic bacteria was suggested. In this study, the inhibitory effect of the probiotic Streptococcus salivarius subsp. salivarius strains M18 and K12, Streptococcus oralis subsp. dentisani 7746, and Lactobacillus reuteri ATCC PTA 5289 on anaerobic periodontal bacteria and Aggregatibacter actinomycetemcomitans was tested. Rarely included in other studies, we also quantified the inverse effect of pathogens on probiotic growth. Probiotics and periodontal pathogens were co-incubated anaerobically in a mixture of autoclaved saliva and brain heart infusion broth. The resulting genome numbers of the pathogens and of the probiotics were measured by quantitative real-time PCR. Mixtures of the streptococcal probiotics were also used to determine their synergistic, additive, or antagonistic effects. The overall best inhibitor of the periodontal pathogens was L. reuteri ATCC PTA 5289, but the effect is coenzyme B12-, anaerobiosis-, as well as glycerol-dependent, and further modulated by L. reuteri strain DSM 17938. Notably, in absence of glycerol, the pathogen-inhibitory effect could even turn into a growth spurt. Among the streptococci tested, S. salivarius M18 had the most constant inhibitory potential against all pathogens, followed by K12 and S. dentisani 7746, with the latter still having significant inhibitory effects on P. intermedia and A. actinomycetemcomitans. Overall, mixtures of the streptococcal probiotics did inhibit the growth of the pathogens equally or–in the case of A. actinomycetemcomitans- better than the individual strains. P. gingivalis and F. nucleatum were best inhibited by pure cultures of S. salivarius K12 or S. salivarius M18, respectively. Testing inverse effects, the growth of S. salivarius M18 was enhanced when incubated with the periodontal pathogens minus/plus other probiotics. In contrast, S. oralis subsp. dentisani 7746 was not much influenced by the pathogens. Instead, it was significantly inhibited by the presence of other streptococcal probiotics. In conclusion, despite some natural limits such as persistence, the full potential for probiotic treatment is by far not utilized yet. Especially, further exploring concerted activity by combining synergistic strains, together with the application of oral prebiotics and essential supplements and conditions, is mandatory.

Candida albicans and Oral Carcinogenesis. A Brief Review

“…This is due to the interactions between microbes and between microbes and host. The presence of microorganisms such as Streptococcus salivarius K12 (secretes a bactericidal inhibitor that inhibits the growth of Gram-negative species associated with periodontitis and halitosis) and others in the normal microflora of the mouth inhibits the colonization by other germs, some of which may be pathogenic [50,51]. Indeed, the use of bacterium therapy with probiotics helps immune defenses and in the concept of eubiosis of the microbiota [51,52].…”

Das orale Mikrobiom – Freund oder Feind? Eine überwiegend naturwissenschaftliche Betrachtung

“…Die zentrale Aufgabe der Zukunft wird also die nachhaltige, persistierende Ansiedlung dieser Keime am Ort des pathologischen Geschehens sein. Dabei könnte es helfen, ihnen einen entscheidenden Selektionsvorteil gegenüber der etablierten Standortflora zu verschaffen, zum Beispiel durch gleichzeitige Gabe von Glycerol (Substrat für Reuterin-Produktion) und Vitamin B 12 (Ko-Faktor der Reuterin-Produktion) im Falle von L. reuteri [18].…”

Oropharyngeal Probiotic ENT-K12 as an Effective Dietary Intervention for Children With Recurrent Respiratory Tract Infections During Cold Season

“…A study using real-time PCR to monitor the persistence of oropharyngeal probiotic ENT-K12 administration in oral cavity indicates that within few days of administration, ENT-K12 typically colonizes various sites of oropharyngeal mucosal membranes including the tongue, buccal, and both sides of pharynx; its simulated bacteriocin can be detected in saliva ( 18 ), plus that the megaplasmid encoding salivaricin A2 and salivaricin B appear to be transmissible between S. salivarius strains with the megaplasmid having been observed to move to another S. salivarius strain in the oral cavity of subjects colonized with strain ENT-K12 ( 19 ), providing its beneficial effect of maintaining oropharyngeal homeostasis and as an antipharyngitis agent ( 20 , 21 ), and the ability of preventing immune activation induced by oral pathogens without altering the native salivary microbiome and inflammatory markers in healthy oral cavity ( 22 ). Furthermore, oropharyngeal probiotic ENT-K12 is able to downregulate immune responses through the action on NF-κB signaling pathways elicited by pathogens, inhibit NF-κB subunit translocating into the nucleus, attenuate IL-8 secretion induced by inflammatory mediators, upregulate genes responsible for activating the interferon signaling pathways with antiviral and cytokine modulation properties, and specifically alter the expression of host genes involved in multiple innate defense pathways, epithelial layer adhesion, and homeostasis pathways, altogether stimulating an anti-inflammatory response and actively protecting the host from inflammation and apoptosis induced by pathogens ( 23 ).…”