Acid tolerance response and survival by oral bacteria

Abstract

Using 21 species of oral bacteria, representing six acidogenic genera, we undertook to determine whether the pH-limiting exponential growth is related to the ability of the organisms to generate an acid-tolerance response that results in enhanced survival at low pH. The lower pH limit of exponential growth varied by more than two units with that of Neisseria A182 at pH 6.34; growth of Lactobacillus casei RB1014 stopped at pH 3.81, with species of Actinomyces, Enterococcus, Prevotella and Streptococcus falling between these limits. The working hypothesis was that the organisms with the higher pH limits for growth are unable to respond to acidic environments in order to survive, whereas the more aciduric organisms would possess or acquire acid tolerance. Adaptation to acid tolerance was tested by determining whether the prior exposure of exponential-phase cells to a low, sub-lethal pH would trigger the induction of a mechanism that would enhance survival at a pH killing pH 7.5 control cells. The killing pH varied from pH 4.5 for Prevotella intermedia ATCC 25611 to pH 2.3 for the three Lactobacillus casei strains in the study, with the three Streptococcus mutans strains killed at pH 3.0 for 3 h. The adaptation experiments revealed three groups of organisms: non-acid-responders, generally representing strains with the highest terminal pH values; weak acid-responders in the middle of the pH list, generating low numbers of survivors at one or two pH values, and the aciduric, strong responders generating a high number of survivors at pH values in the range 6.0 to 3.5, but not at pH 7.5. Predominant among the latter group were the S. mutans and Lactobacilli casei strains, with the most significant adaptive response exhibited by S. mutans LT11 and S. mutans Ingbritt, involving a process that required protein synthesis. Time course experiments with the latter organisms indicated that 90-120 min was required after exposure to the triggering pH before the acid response was fully functional. These results indicate that the sudden exposure of strains of oral streptococci and lactobacilli, as well as Enterococcus faecalis, to pH values between 6.0 and 3.5 results in the induction of an acid tolerance response that enhances the survival of these strains at or below pH 3.5.

Acid-resistant genes of oral plaque microbiome from the functional metagenomics

“…Currently, various meticulous investigations on the molecular and physiological responses to acid shock are limited to cultivable oral bacteria [25], such as S. mutans , the gastric inhabitant E. coli [26] and Helicobacter pylori [27]. However, knowledge regarding the aciduric features of so far uncultivable microorganisms remains scarce.…”

Antimicrobial peptide GH12 suppresses cariogenic virulence factors of Streptococcus mutans

“…S. mutans UA159 was obtained from the State Key Laboratory of Oral Diseases at Sichuan University (Chengdu, China) and grown in brain–heart infusion broth (BHI; Oxoid, Basingstoke, Hampshire, UK) anaerobically (85% N 2 , 10% H 2 and 5% CO 2 ) at 37°C [22]. For lactic acid measurement, buffered peptone water (BPW, Nissui, Tokyo, Japan) was used [23], and for acid tolerance assays, tryptone-yeast extract medium containing 20 mM glucose (TYEG) was applied [24]. …”

“…The effect of GH12 on the acid tolerance of S. mutans was evaluated by measuring the viability of bacteria after 120 min exposure of pH 5.0 [24]. S. mutans was grown in TYEG broth until mid-logarithmic phase.…”

Protein Expression by Streptococcus mutans during Initial Stage of Biofilm Formation

“…These cells not only expressed different proteins but also were physiologically different in terms of acid tolerance, with 41.5% of the biofilm cells surviving an acid shock of pH 3.0 compared to only 4 ϫ 10 Ϫ5 % of the planktonic cells (39). S. mutans is know to induce an acid tolerance response (ATR) at sublethal pH values (ϳ5.5) that enhances survival at lower pH values (36). Exposing the 3-day biofilm cells to pH 5.5 for 2 h only induced a negligible ATR and didn't increase the number of survivors, suggesting that surface growth itself triggered an ATR in biofilm cells sometime during biofilm development (39).…”