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DAMPs and NETs in Sepsis
Naomi-Liza Denning1,2,3, Monowar Aziz1,2, Steven D Gurien1,3
1Center for Immunology and Inflammation, Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Abstract:
Sepsis is a deadly inflammatory syndrome caused by an exaggerated immune response to infection. Much has been focused on host response to pathogens mediated through the interaction of pathogen-associated molecular patterns (PAMPs) and pattern recognition receptors (PRRs). PRRs are also activated by host nuclear, mitochondrial, and cytosolic proteins, known as damage-associated molecular patterns (DAMPs) that are released from cells during sepsis. Some well described members of the DAMP family are extracellular cold-inducible RNA-binding protein (eCIRP), high mobility group box 1 (HMGB1), histones, and adenosine triphosphate (ATP). DAMPs are released from the cell through inflammasome activation or passively following cell death. Similarly, neutrophil extracellular traps (NETs) are released from neutrophils during inflammation. NETs are webs of extracellular DNA decorated with histones, myeloperoxidase, and elastase. Although NETs contribute to pathogen clearance, excessive NET formation promotes inflammation and tissue damage in sepsis. Here, we review DAMPs and NETs and their crosstalk in sepsis with respect to their sources, activation, release, and function. A clear grasp of DAMPs, NETs and their interaction is crucial for the understanding of the pathophysiology of sepsis and for the development of novel sepsis therapeutics.
Insights
Sepsis involves damage-associated molecular patterns (DAMPs) and neutrophil extracellular traps (NETs) that promote inflammation. Understanding their interaction is key to developing new sepsis treatments.
Area of Science:
- Immunology
- Pathophysiology
- Molecular Biology
Background:
- Sepsis is a life-threatening inflammatory condition driven by an overactive immune response to infection.
- Host immune responses involve pathogen-associated molecular patterns (PAMPs) interacting with pattern recognition receptors (PRRs).
- Pattern recognition receptors (PRRs) also recognize damage-associated molecular patterns (DAMPs) released from damaged host cells during sepsis.
Purpose of the Study:
- To review damage-associated molecular patterns (DAMPs) and neutrophil extracellular traps (NETs) in sepsis.
- To elucidate the crosstalk between DAMPs and NETs in sepsis pathophysiology.
- To highlight the importance of understanding DAMPs and NETs for developing novel sepsis therapeutics.
Main Methods:
- Literature review of DAMPs and NETs in sepsis.
- Analysis of DAMPs and NETs sources, activation, release, and function.
- Examination of the interplay between DAMPs and NETs.
Main Results:
- DAMPs, including eCIRP, HMGB1, histones, and ATP, are released from cells via inflammasome activation or cell death.
- Neutrophil extracellular traps (NETs) are DNA webs released by neutrophils, containing histones and enzymes.
- Both DAMPs and excessive NETs contribute to sepsis-induced inflammation and tissue damage.
Conclusions:
- DAMPs and NETs are critical components of the inflammatory response in sepsis.
- The interaction and crosstalk between DAMPs and NETs significantly contribute to sepsis pathophysiology.
- A comprehensive understanding of DAMPs and NETs is essential for advancing sepsis treatment strategies.
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