The Role of Reactive-Oxygen-Species in Microbial Persistence and Inflammation
AbstractThe mechanisms of chronic infections caused by opportunistic pathogens are of keen interest to both researchers and health professionals globally. Typically, chronic infectious disease can be characterized by an elevation in immune response, a process that can often lead to further destruction. Reactive-Oxygen-Species (ROS) have been strongly implicated in the aforementioned detrimental response by host that results in self-damage. Unlike excessive ROS production resulting in robust cellular death typically induced by acute infection or inflammation, lower levels of ROS produced by host cells are increasingly recognized to play a critical physiological role for regulating a variety of homeostatic cellular functions including growth, apoptosis, immune response, and microbial colonization. Sources of cellular ROS stimulation can include “danger-signal-molecules” such as extracellular ATP (eATP) released by stressed, infected, or dying cells. Particularly, eATP-P2X7 receptor mediated ROS production has been lately found to be a key modulator for controlling chronic infection and inflammation. There is growing evidence that persistent microbes can alter host cell ROS production and modulate eATP-induced ROS for maintaining long-term carriage. Though these processes have yet to be fully understood, exploring potential positive traits of these “injurious” molecules could illuminate how opportunistic pathogens maintain persistence through physiological regulation of ROS signaling. View Full-Text
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Spooner, R.; Yilmaz, Ö. The Role of Reactive-Oxygen-Species in Microbial Persistence and Inflammation. Int. J. Mol. Sci. 2011, 12, 334-352.
Spooner R, Yilmaz Ö. The Role of Reactive-Oxygen-Species in Microbial Persistence and Inflammation. International Journal of Molecular Sciences. 2011; 12(1):334-352.Chicago/Turabian Style
Spooner, Ralee; Yilmaz, Özlem. 2011. "The Role of Reactive-Oxygen-Species in Microbial Persistence and Inflammation." Int. J. Mol. Sci. 12, no. 1: 334-352.