Department of Translational Research, New Technologies in Medicine Surgery, University of Pisa, Italy.
Department of Biomolecular Sciences, Division of Toxicological, Hygiene and Environmental Sciences, University of Urbino "Carlo Bo", via S. Chiara 27, 61029 Urbino, PU, Italy.
Arch Oral Biol. 2017 Jun;78:48-57. doi: 10.1016/j.archoralbio.2017.02.004. Epub 2017 Feb 4.
This research investigates the ability of live and heat-killed (HK) Lactic Acid Bacteria (LAB) to interfere with Streptococcus mutans ATCC 25175 and Streptococcus oralis ATCC 9811 during biofilm formation.
Eight Lactobacillus spp. and two oral colonizers, pathogenic Streptococcus mutans and resident Streptococcus oralis, were characterized for their aggregation abilities, cell surface properties and biofilm formation ability on titanium surface. Then, the interference activity of selected live and HK Lactobacillus spp. during S. mutans and S. oralis biofilm development were performed. The cell-free culture supernatants (CFCS) anti-biofilm activity was also determined.
LAB possess good abilities of auto-aggregation (from 14.19 to 28.97%) and of co-aggregation with S. oralis. The cell-surfaces characteristics were most pronounced in S. mutans and S. oralis, while the highest affinities to xylene and chloroform were observed in Lactobacillus rhamnosus ATCC 53103 (56.37%) and Lactobacillus paracasei B21060 (43.83%). S. mutans and S. oralis developed a biofilm on titanium surface, while LAB showed a limited or no ability to create biofilm. Live and HK L. rhamnosus ATCC 53103 and L. paracasei B21060 inhibited streptococci biofilm formation by competition and displacement mechanisms with no substantial differences. The CFCSs of both LAB strains, particularly the undiluted one of L. paracasei B21060, decreased S. mutans and S. oralis biofilm formation.
This study evidenced the association of LAB aggregation abilities and cell-surface properties with the LAB-mediated inhibition of S. mutans and S. oralis biofilm formation. Lactobacilli showed different mechanisms of action and peculiar strain-specific characteristics, maintained also in the heat-killed LAB.
本研究旨在探讨活菌和热灭活（HK）乳酸菌（LAB）在形成生物膜过程中对变异链球菌 ATCC 25175 和口腔常驻菌乳杆菌 ATCC 9811 的干扰能力。
对 8 株乳杆菌和 2 株口腔定植菌，即致病性变异链球菌和常驻乳杆菌，进行聚集能力、细胞表面特性和钛表面生物膜形成能力的表征。然后，研究了选定的活菌和 HK 乳杆菌在变异链球菌和乳杆菌生物膜形成过程中的干扰活性。同时还测定了无细胞培养上清液（CFCS）的抗生物膜活性。
LAB 具有良好的自聚集能力（14.19%~28.97%）和与乳杆菌的共聚集能力。细胞表面特性在变异链球菌和乳杆菌中最为明显，而对二甲苯和氯仿的亲和力最高的是鼠李糖乳杆菌 ATCC 53103（56.37%）和副干酪乳杆菌 B21060（43.83%）。变异链球菌和乳杆菌在钛表面形成生物膜，而 LAB 则显示出有限或无法形成生物膜的能力。活菌和 HK 鼠李糖乳杆菌 ATCC 53103 和副干酪乳杆菌 B21060 通过竞争和置换机制抑制链球菌生物膜形成，无明显差异。两种 LAB 菌株的 CFCS，特别是副干酪乳杆菌 B21060 的未稀释 CFCS，均可降低变异链球菌和乳杆菌生物膜的形成。
本研究证明了 LAB 聚集能力和细胞表面特性与 LAB 介导的抑制变异链球菌和乳杆菌生物膜形成之间的关联。乳杆菌表现出不同的作用机制和独特的菌株特异性特征，在热灭活 LAB 中也得到了保持。
