About this Research Topic
The innate immune system constitutes the first line of host defense during infection, hence it plays a pivotal role in the early recognition of microbes and subsequent initiation of a pro-inflammatory response to invading pathogens.
The innate immune system is mainly centered on the physical and chemical barriers to infection, in addition to different cell types known to recognize invading pathogens and activate antimicrobial immune responses. Physical and chemical defense mechanisms include the epidermis, the ciliated respiratory epithelium, the vascular endothelium, and various mucosal surfaces with antimicrobial secretions. The cellular components of innate immunity include antigen-presenting dendritic cells, phagocytic macrophages and granulocytes, cytotoxic natural killer cells, and lymphocytes. The important ability of the innate immune system to recognize and limit microbes early during infection is primarily based on employment of complement activation, phagocytosis, autophagy, and activation of various immune cells in order to ensure a successful host defense mechanism against microbial pathogens.
Activation of various immune cells requires an appropriate recognition and sensing of the pathogen-associated molecular patterns (PAMPs) by a range of pattern recognition receptors (PPRs) expressed by the immune cells, followed by the initiation of an intricate signaling cascade. This cascade results in an inflammatory process that involves recruitment of various leukocytes to the site of infection, activation of antimicrobial effector mechanisms, and subsequently, induction of an adaptive immune response that will ultimately promote the clearance of infection.
However, various microbial pathogens have developed elegant strategies to evade the innate immune system. Those mechanisms are widely diverse and occur at all the steps of the host infection process. Those strategies include but are not limited to:
• Evasion of the frontline barriers.
• Adhesion to epithelial cells and proliferation on their surfaces.
• Alteration of their PAMPs to become less immunogenic.
• Exploitation of the host cytoskeleton and membranous structures in order to invade and/or gain access inside the infected host cell.
• Establishment and maintenance of an intracellular niche inside the infected cell.
• Interference with the host signaling cascade by distorting the balance between positive and negative signals or through activation of anti-inflammatory responses that are induced by different virulence factors.
In the last few years a great effort has been made to understand the molecular mechanisms governing this subversion, and various host factors and bacterial virulence factors were identified.
The objective of this research topic is to discuss known strategies of bacterial evasion from the innate immune system, to tackle the complexity of those strategies, and to uncover novel mechanisms that may be involved.
The innate immune system is mainly centered on the physical and chemical barriers to infection, in addition to different cell types known to recognize invading pathogens and activate antimicrobial immune responses. Physical and chemical defense mechanisms include the epidermis, the ciliated respiratory epithelium, the vascular endothelium, and various mucosal surfaces with antimicrobial secretions. The cellular components of innate immunity include antigen-presenting dendritic cells, phagocytic macrophages and granulocytes, cytotoxic natural killer cells, and lymphocytes. The important ability of the innate immune system to recognize and limit microbes early during infection is primarily based on employment of complement activation, phagocytosis, autophagy, and activation of various immune cells in order to ensure a successful host defense mechanism against microbial pathogens.
Activation of various immune cells requires an appropriate recognition and sensing of the pathogen-associated molecular patterns (PAMPs) by a range of pattern recognition receptors (PPRs) expressed by the immune cells, followed by the initiation of an intricate signaling cascade. This cascade results in an inflammatory process that involves recruitment of various leukocytes to the site of infection, activation of antimicrobial effector mechanisms, and subsequently, induction of an adaptive immune response that will ultimately promote the clearance of infection.
However, various microbial pathogens have developed elegant strategies to evade the innate immune system. Those mechanisms are widely diverse and occur at all the steps of the host infection process. Those strategies include but are not limited to:
• Evasion of the frontline barriers.
• Adhesion to epithelial cells and proliferation on their surfaces.
• Alteration of their PAMPs to become less immunogenic.
• Exploitation of the host cytoskeleton and membranous structures in order to invade and/or gain access inside the infected host cell.
• Establishment and maintenance of an intracellular niche inside the infected cell.
• Interference with the host signaling cascade by distorting the balance between positive and negative signals or through activation of anti-inflammatory responses that are induced by different virulence factors.
In the last few years a great effort has been made to understand the molecular mechanisms governing this subversion, and various host factors and bacterial virulence factors were identified.
The objective of this research topic is to discuss known strategies of bacterial evasion from the innate immune system, to tackle the complexity of those strategies, and to uncover novel mechanisms that may be involved.
Keywords: immune, pathogens, infection, innate immune system, antimicrobial immune response
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