Neutrophil extracellular traps in bacterial infections and evasion strategies

Abstract

Neutrophils are innate immune cells that have a vital role in host defense systems. Neutrophil extracellular traps (NETs) are one of neutrophils’ defense mechanisms against pathogens. NETs comprise an ejected lattice of chromatin associated with histones, granular proteins, and cytosolic proteins. They are thought to be an efficient strategy to capture and/or kill bacteria and received intensive research interest in the recent years. However, soon after NETs were identified, it was observed that certain bacteria were able to evade NET entrapment through many different mechanisms. Here, we outline the recent progress of NETs in bacterial infections and the strategies employed by bacteria to evade or withstand NETs. Identifying the molecules and mechanisms that modulate NET release will improve our understanding of the functions of NETs in infections and provide new avenues for the prevention and treatment of bacterial diseases.

Inflammatory Cytokines and Chemokines Are Synergistically Induced in a ROS-Dependent Manner by a Co-Culture of Corneal Epithelial Cells and Neutrophil-like Cells in the Presence of Particulate Matter

“…Although a disruption of immune cells (neutrophils) was not evident under the microscope, it is thought that Neutrophil Extracellular Traps (NETs) [38,39], one of the characteristics of neutrophils, are formed within this system. NETs have been identified as triggers for a self-limited inflammatory reaction [40].…”

An inflammatory paradox: strategies inflammophilic oral pathobionts employ to exploit innate immunity via neutrophil manipulation

“…Through a process called NETosis, neutrophils elaborate structures comprised of extracellular fibers of chromatin and granular proteins that are able to trap and kill pathogens ( 47 ). While an effective defense against most microbes, a number of bacteria have evolved strategies to subvert NET production or function ( 48 ).…”

“…The ability of microbes to use compounds recognized as “self” molecules like hyaluronan and sialoglycoproteins supports signaling through host-specific pathways and demonstrates an ingenious form of molecular mimicry to undermine host defenses. Many microbes naturally promote NETosis as a consequence of their inherent pro-inflammatory nature ( 48 ). For those that have evolved ways to resist NET-dependent killing, the formation of NETs themselves may even be beneficial due to its aggravation of the inflammatory response ( 59 ).…”