Abstract
To ensure a functional immune system, the mammalian host must detect and respond to the presence of pathogenic bacteria during infection. This is accomplished in part by generating reactive oxygen species (ROS) that target invading bacteria; a process that is facilitated by NADPH oxidase upregulation. Thus, bacterial pathogens must overcome the oxidative burst produced by the host innate immune cells in order to survive and proliferate. In this way, pathogenic bacteria develop virulence, which is related to the affinity to secrete effector proteins against host ROS in order to facilitate microbial survival in the host cell. These effectors scavenge the host generated ROS directly, or alternatively, manipulate host cell signaling mechanisms designed to benefit pathogen survival. The redox-balance of the host is important for the regulation of cell signaling activities that include mitogen-activated protein kinase (MAPK), p21-activated kinase (PAK), phosphatidylinositol 3-kinase (PI3K)/Akt, and nuclear factor κB (NF-κB) pathways. An understanding of the function of pathogenic effectors to divert host cell signaling is important to ascertain the mechanisms underlying pathogen virulence and the eventual host–pathogen relationship. Herein, we examine the effectors produced by the microbial secretion system, placing emphasis on how they target molecular signaling mechanisms involved in a host immune response. Moreover, we discuss the potential impact of bioactive polyphenols in modulating these molecular interactions that will ultimately influence pathogen virulence.
Highlights
An innate immune system will respond to a pathogenic bacterium-induced mammalian infection
Once the bacteria invade the host cell, they are exposed to a variety of killing mechanisms that include exposure to reactive oxygen species (ROS) generated by a respiratory burst response
Yersinia is a pathogenic bacteria responsible for the plague known as the Black Death
Summary
An innate immune system will respond to a pathogenic bacterium-induced mammalian infection. To survive and successfully enter a host cell, bacteria must release specific protein(s) and virulence factors that function to overcome host cellular signaling defense mechanisms that affect the immune response. Virulence factors refer to a toxin, or a protein that is released by the pathogen to facilitate infecting the host [6]. Pathogens secrete a variety of effector proteins with varying activities as a defense mechanism to enhance survival in host cells and promote bacterial virulence. This usually occurs by enhancing attachment to eukaryotic cells, scavenging toxic ROS, or intoxicating target cells that assist in survival [1]. There are few studies to show that some phenolic compounds can affect the secretion system of pathogenic bacteria, which in turn influences virulence and facilitates pathogenicity
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