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.2020 Aug 20;12(1):1805553.
doi: 10.1080/20002297.2020.1805553.

Probiotics alter biofilm formation and the transcription ofPorphyromonas gingivalis virulence-associated genes

Affiliations

Probiotics alter biofilm formation and the transcription ofPorphyromonas gingivalis virulence-associated genes

Karin Hitomi Ishikawa et al. J Oral Microbiol..

Abstract

Background and objective: The potential of probiotics on the prevention and control of periodontitis and other chronic inflammatory conditions has been suggested.Lactobacillus andBifidobacterium species influenceP. gingivalis interaction with gingival epithelial cells (GECs) but may not act in a unique way. In order to select the most appropriate probiotic againstP. gingivalis, we aimed to evaluate the effect of several strains onPorphyromonas gingivalis biofilm formation and transcription virulence-associated factors (PgVAFs).

Methods: Cell-free pH neutralized supernatants (CFS) and livingLactobacillus spp. andBifidobacterium spp. were tested againstP. gingivalis ATCC 33277 and W83, in mono- and multi-species (withStreptococcus oralis andS. gordonii) biofilms. Relative transcription ofP. gingivalis genes (fimA, mfa1, kgp, rgp, ftsH andluxS) was determined in biofilms and under GECs co-infection.

Results: Probiotics CFS reducedP. gingivalis ATCC 33277 levels in mono-species biofilms and living probiotics reducedP. gingivalis abundance in multi-species biofilms.L. acidophilus LA5 down-regulated transcription of most PgVAFs in biofilms and GECs.

Conclusions: Probiotics affectP. gingivalis biofilm formation by down-regulating overall PgVAFs with the most pronounced effect observed forL. acidophilus LA5.

Keywords: Probiotics; biofilm; fimbriae; gene expression; gingipain; periodontitis.

© 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

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Conflict of interest statement

The authors report no conflicts of interest related to this study.

Figures

Figure 1.
Figure 1.
Effect of probiotics cell-free supernatants (CFS) diluted at 1:2.5 onP. gingivalis W83 (a1, mono-species; a2, multi-species) and ATCC 33277 (b1, mono-species; b2, multi-species) biofilm biomass, represented by the OD490nm of the standard biofilm dye. Groups: Neg. control- Negative control represents non-inoculated medium; Control- CFS-free positive controls ofP. gingivalis mono- and multi-species biofilms (So –S. oralis and Sg –S. gordonii), and experimental group with CFS of: LA5 –L. acidophilus LA5, HN001 –L. rhamnosus HN001, DSM –L. reuteri DSM 17938, 1101A –B. breve 1101A, 1191A –B. pseudolongum 1191A and 1622A –B. bifidum 1622A. Experiments were conducted in triplicate. (*) Statistically significant difference when compared to respective positive controls using One-way ANOVA with post hoc Tukey’s multiple comparisons (p < 0.05).
Figure 2.
Figure 2.
Effect of probiotics cell-free supernatants (CFS of LA5 –L. acidophilus LA5, HN001 –L. rhamnosus HN001, DSM –L. reuteri DSM 17938, 1101A –B. breve 1101A, 1191A –B. pseudolongum 1191A and 1622A –B. bifidum 1622A) on the relative abundance ofP. gingivalis W83 (a) or ATCC 33277 (b) and the initial colonizersS. oralis andS. gordonii in multi-species biofilms, represented as the mean percentage of each bacteria determined by qPCR. (*) Significant difference inP. gingivalis counts when compared to respective positive controls using One-way ANOVA with post hoc Tukey’s multiple comparisons (p < 0.05).
Figure 3.
Figure 3.
Effect of livingLactobacillus sp (L. acidophilus LA5,L. rhamnosus HN001,L. reuteri DSM 17938) andBifidobacterium sp (B. breve 1101A,B. pseudolongum 1191A andB. bifidum 1622A) on the relative abundance ofP. gingivalis W83 (a) or ATCC 33277 (b) and the initial colonizersS. oralis andS. gordonii after cell-to-cell interaction, represented as the mean percentage of each bacteria determined by qPCR (*). Significant difference inP. gingivalis abundance, when compared to respective positive controls using One-way ANOVA with post hoc Tukey’s multiple comparisons (p <0.05).
Figure 4.
Figure 4.
Effect of probiotics on the relative transcription ofP. gingivalis encoding virulence genes (mfa1 – minor fimbriae; fimA – major fimbriae; kgp – lysine gingipain; rgpA – arginine gingipain; ftsH – metalloproteinase, and luxS – quorum sensing components), determined by RT-qPCR.P. gingivalis strains W83 and ATCC 33277 biofilms formed in BHIHM broth added with the supernatant of cultures of probiotics (a1 and a2 -L. acidophilus LA5, b1 and b2 –L. rhamnosus HN001, c1 and c2 –L. reuteri DSM 17938, d1 and d2 –B. breve 1101A, e1 and e2 –B. pseudolongum 1191A and f1 and f2 –B. bifidum 1622A) diluted to 1:2.5, in mono-species (a1, b1, c1, d1, 1 and f1) and multi-species (a2, b2, c2, d2, e2 and f2), and infecting OBA-9 GECs with probiotic co-infection at a MOI of 1:1,000 (a3 -L. acidophilus LA5, b3 –L. rhamnosus HN001, c3 –L. reuteri DSM 17938, d3 –B. breve 1101A, e3 –B. pseudolongum 1191A and f3 –B. bifidum 1622A). Data are expressed as fold changes in relation to positive control conditions (biofilms without probiotic cell-free supernatants or GECs without probiotic bacteria), after normalization to the endogenous control gene16SrRNA. (*) Significant difference when compared to respective positive controls using One-way ANOVA with post hoc Tukey’s multiple comparisons (p < 0.05).
Figure 4.
Figure 4.
(Continued).
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Grants and funding

This study was supported by the FAPESP under [grant 2015/18273-9]. KHI, DK and EAS were supported by FAPESP scholarships [2016/13156-7, 2016/13159-6 and 2016/14687-6], respectively. DM undergraduate scholarship was supported by CNPq.

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