scholarly journals Acid Stress Survival Mechanisms of the Cariogenic Bacterium Streptococcus mutans

Author(s):  
Yoshihisa Yamashita ◽  
Yukie Shibat
2009 ◽  
Vol 75 (24) ◽  
pp. 7838-7849 ◽  
Author(s):  
Dharanesh Gangaiah ◽  
Issmat I. Kassem ◽  
Zhe Liu ◽  
Gireesh Rajashekara

ABSTRACT Campylobacter jejuni, a gram-negative, microaerophilic bacterium, is a predominant cause of bacterial gastroenteritis in humans. Although considered fragile and fastidious and lacking many classical stress response mechanisms, C. jejuni exhibits a remarkable capacity for survival and adaptation, successfully infecting humans and persisting in the environment. Consequently, understanding the physiological and genetic properties that allow C. jejuni to survive and adapt to various stress conditions is crucial for therapeutic interventions. Of importance is polyphosphate (poly-P) kinase 1 (PPK1), which is a key enzyme mediating the synthesis of poly-P, an essential molecule for survival, mediating stress responses, host colonization, and virulence in many bacteria. Therefore, we investigated the role of PPK1 in C. jejuni pathogenesis, stress survival, and adaptation. Our findings demonstrate that a C. jejuni Δppk1 mutant was deficient in poly-P accumulation, which was associated with a decreased ability to form viable-but-nonculturable cells under acid stress. The Δppk1 mutant also showed a decreased frequency of natural transformation and an increased susceptibility to various antimicrobials. Furthermore, the Δppk1 mutant was characterized by a dose-dependent deficiency in chicken colonization. Complementation of the Δppk1 mutant with the wild-type copy of ppk1 restored the deficient phenotypes to levels similar to those of the wild type. Our results suggest that poly-P plays an important role in stress survival and adaptation and might contribute to genome plasticity and the spread and development of antimicrobial resistance in C. jejuni. These findings highlight the potential of PPK1 as a novel target for therapeutic interventions.


Microbiology ◽  
1999 ◽  
Vol 145 (2) ◽  
pp. 357-366 ◽  
Author(s):  
Juan A. Gutierrez ◽  
Paula J. Crowley ◽  
Dennis G. Cvitkovitch ◽  
L. Jeannine Brady ◽  
Ian R. Hamilton ◽  
...  

2012 ◽  
Vol 79 (5) ◽  
pp. 1436-1443 ◽  
Author(s):  
Kei Fujishima ◽  
Miki Kawada-Matsuo ◽  
Yuichi Oogai ◽  
Masayuki Tokuda ◽  
Mitsuo Torii ◽  
...  

ABSTRACTLarge numbers of bacteria coexist in the oral cavity.Streptococcus sanguinis, one of the major bacteria in dental plaque, produces hydrogen peroxide (H2O2), which interferes with the growth of other bacteria.Streptococcus mutans, a cariogenic bacterium, can coexist withS. sanguinisin dental plaque, but to do so, it needs a means of detoxifying the H2O2produced byS. sanguinis. In this study, we investigated the association of three oxidative stress factors, Dpr, superoxide dismutase (SOD), and AhpCF, with the resistance ofS. sanguinisto H2O2. The knockout ofdprandsodsignificantly increased susceptibility to H2O2, while the knockout ofahpCFhad no apparent effect on susceptibility. In particular,dprinactivation resulted in hypersensitivity to H2O2. Next, we sought to identify the factor(s) involved in the regulation of these oxidative stress genes and found that PerR negatively regulateddprexpression. The knockout ofperRcaused increaseddprexpression levels, resulting in low-level susceptibility to H2O2compared with the wild type. Furthermore, we evaluated the roles ofperR,dpr, andsodwhenS. mutanswas cocultured withS. sanguinis. Culturing of thedprorsodmutant withS. sanguinisshowed a significant decrease in theS. mutanspopulation ratio compared with the wild type, while theperRmutant increased the ratio. Our results suggest thatdprandsodinS. mutansare involved in coexistence withS. sanguinis, and PerR is associated with resistance to H2O2in regulating the expression of Dpr.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yaqi Wang ◽  
Wei Cao ◽  
Justin Merritt ◽  
Zhoujie Xie ◽  
Hao Liu

FtsH belongs to the AAA+ ATP-dependent family of proteases, which participate in diverse cellular processes and are ubiquitous among bacteria, chloroplasts, and mitochondria. FtsH is poorly characterized in most organisms, especially compared to other major housekeeping proteases. In the current study, we examined the source of FtsH essentiality in the human oral microbiome species Streptococcus mutans, one of the primary etiological agents of dental caries. By creating a conditionally lethal ftsH mutant, we were able to identify a secondary suppressor missense mutation in the vicR gene, encoding the response regulator of the essential VicRK two-component system (TCS). Transcriptomic analysis of the vicR (G195R) mutant revealed significantly reduced expression of 46 genes, many of which were located within the genomic island Tnsmu2, which harbors the mutanobactin biosynthetic gene cluster. In agreement with the transcriptomic data, deletion of the mutanobactin biosynthetic gene cluster suppressed ftsH essentiality in S. mutans. We also explored the role of FtsH in S. mutans physiology and demonstrated its critical role in stress tolerance, especially acid stress. The presented results reveal the first insights within S. mutans for the pleiotropic regulatory function of this poorly understood global regulator.


2018 ◽  
Vol 53 (1) ◽  
pp. 84-95 ◽  
Author(s):  
Kyungsun Kim ◽  
Jung-Sub An ◽  
Bum-Soon Lim ◽  
Sug-Joon Ahn

Bisphenol A glycidyl methacrylate (bis-GMA), which is released into the oral environment by dental composites through incomplete polymerization, hydrolysis, and mechanical degradation, can significantly influence oral ecology around resin-based materials. The purpose of this study was to investigate how bis-GMA changes the virulence properties of Streptococcus mutans, a major cariogenic bacterium in humans. The results show that bis-GMA not only inhibited the planktonic growth of cells in medium containing glucose, fructose, or mannose, but also reduced the viability of S. mutans. However, the presence of bis-GMA increased sugar transport and intracellular polysaccharide accumulation in S. mutans, thereby increasing the potential of cell persistence. In addition, bis-GMA could enhance S. mutans’s adhesion to hard surfaces and glucan synthesis, which could contribute to biofilm formation. Although free bis-GMA made cells vulnerable to acidic stress, it also provided increased resistance to hydrogen peroxide, which might confer an advantage in competition with other oral microorganisms during the early stage of biofilm development. Interestingly, the presence of bis-GMA did not change the ability of S. mutans to interact with saliva. The results suggest that leachable bis-GMA could contribute to biofilm-related secondary dental caries at the marginal interface between resin-based materials and teeth by altering the virulent properties of S. mutans, although bis-GMA reduced the planktonic growth and viability of S. mutans.


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