Stress responses in Streptococcus species and their effects on the host

Abstract

Streptococci cause a variety of diseases, such as dental caries, pharyngitis, meningitis, pneumonia, bacteremia, endocarditis, erysipelas, and necrotizing fasciitis. The natural niche of this genus of bacteria ranges from the mouth and nasopharynx to the skin, indicating that the bacteria will inevitably be subjected to environmental changes during invasion into the host, where it is exposed to the host immune system. Thus, the Streptococcus-host interaction determines whether bacteria are cleared by the host's defenses or whether they survive after invasion to cause serious diseases. If this interaction was to be deciphered, it could aid in the development of novel preventive and therapeutic agents. Streptococcus species possess many virulent factors, such as peroxidases and heat-shock proteins (HSPs), which play key roles in protecting the bacteria from hostile host environments. This review will discuss insights into the mechanism(s) by which streptococci adapt to host environments. Additionally, we will address how streptococcal infections trigger host stress responses; however, the mechanism by which bacterial components modulate host stress responses remains largely unknown.

Relationship between dental caries and metabolic syndrome among 13 998 middle‐aged urban Chinese

“…31,32 Although not well understood, several underlying mechanisms have been proposed: the release of inflammatory mediators (interleukin-1α and -1β and tumor necrosis factor-α) into the circulation that play key role in atherogenesis 33 results in macrophage stimulation by the lipopolysaccharides of these microorganisms, 34 enhancing platelet aggregation and thereby increasing the risk of thrombosis, 35 triggering host stress responses in endothelial cells. 36 The number of teeth with caries was associated with increased MetS risk in univariate analysis, and remained statistically significant despite the fact that the effect size was attenuated after adjustment for explanatory variables. Supporting our results, a recent study has shown that the number of teeth with caries and systemic exposure to A. actinomycetemcomitans are associated with several components of MetS.…”

“…Endogenous bacteria (most prominently Streptococcus mutans and Streptococcus sobrinus, as well as lactobacilli) in the biofilm produce weak organic acids as a byproduct of the metabolism of fermentable carbohydrates. 36 The number of teeth with caries was associated with increased MetS risk in univariate analysis, and remained 30 One explanation for this association may be that the number of teeth with caries is a surrogate marker for the lifetime accumulation of oral infections. Over recent decades, accumulating epidemiologic data indicate that common oral diseases, such as caries, periodontal diseases, and the loss of teeth, are associated with MetS, cardiovascular diseases, and diabetes.…”

Cytoprotective effects of cerium and selenium nanoparticles on heat-shocked human dermal fibroblasts: an in vitro evaluation

“…Generally, heat shock proteins (HSPs) play crucial roles in protecting cells against environmental stresses, such as heat shock, low serum, chemicals, and pathogenic bacteria. 3,4 Among the HSP family, the 70 kDa HSPs are the most responsible for intracellular chaperone and extracellular immunoregulatory functions.…”

Identification of an Autorepressing Two-Component Signaling System That Modulates Virulence in Streptococcus suis Serotype 2

“…T o survive in diverse environments, bacteria must sense and respond to external stimuli. Two-component signaling systems (TCSs) are ubiquitous in prokaryotes and represent a major mechanism through which bacterial cells adapt to environmental changes (1,2). A typical TCS consists of a membrane-bound sensor histidine kinase (HK) and a cytoplasmic response regulator (RR) (1).…”

“…Once the mucosal barriers are breached, the bacteria disseminate to different organs and tissues by the bloodstream. TCSs are usually employed to sense and respond to extracellular signals during the infection process (2,9). Bioinformatics analysis of the genome of SS2 strains identified 15 TCSs (10), among which RevS, Salk/SalR, CovR, CiaRH, Ihk/Irr, VirR/VirS, NisK/NisR, 1910HK/RR, and VraSR SS have been reported to regulate the expression of putative virulence factors, mediate multidrug resistance, or alter bacterial metabolism (11)(12)(13)(14)(15)(16)(17)(18)(19)(20), thereby contributing to the adaption of SS2 strains to environmental stimuli.…”