Staphylococcal response to oxidative stress

Abstract

Staphylococci are a versatile genus of bacteria that are capable of causing acute and chronic infections in diverse host species. The success of staphylococci as pathogens is due in part to their ability to mitigate endogenous and exogenous oxidative and nitrosative stress. Endogenous oxidative stress is a consequence of life in an aerobic environment; whereas, exogenous oxidative and nitrosative stress are often due to the bacteria's interaction with host immune systems. To overcome the deleterious effects of oxidative and nitrosative stress, staphylococci have evolved protection, detoxification, and repair mechanisms that are controlled by a network of regulators. In this review, we summarize the cellular targets of oxidative stress, the mechanisms by which staphylococci sense oxidative stress and damage, oxidative stress protection and repair mechanisms, and regulation of the oxidative stress response. When possible, special attention is given to how the oxidative stress defense mechanisms help staphylococci control oxidative stress in the host.

The Use of Starter Cultures in Traditional Meat Products

“…S. xylosus responded to the osmotic stress caused by the addition of salt (NaCl) by overexpressing genes involved in transport and synthesis of osmoprotectants, particularly glycine betaine, and Na + and H + extrusion [185]. To overcome the damaging effects of oxidative and nitrosative stress, staphylococci have developed protection, detoxification, and repair mechanisms controlled by a network of regulators [186].…”

Bacteriolyses of Bacterial Cell Walls by Cu(II) and Zn(II) Ions Based on Antibacterial Results of Dilution Medium Method and Halo Antibacterial Test

“…-and H 2 O 2 permeate into membrane and cytoplasm, that DNA molecular is damaged by oxidative stress [31]. For the penetration of zinc ions to PGN cell wall, the ROS production such as superoxide anion radical O figure 5, the activations of amidase enzyme of N-terminal and endopeptidase enzyme of C-terminal are enhanced [17,18].…”

Catalase Expression Is Modulated by Vancomycin and Ciprofloxacin and Influences the Formation of Free Radicals in Staphylococcus aureus Cultures

“…Within the eukaryotic host, reactive oxygen species, such as hydrogen peroxide, are produced as part of the innate immune response (45). The primary host defense against S. aureus is represented by the neutrophils, which rely on ROS for antimicrobial activity (46). Since our results show that antibiotics influence catalase expression, this modulation may affect the efficacy of antimicrobial therapy.…”