About this Research Topic
Damage-associated molecular patterns (DAMPs) became a fascinating new topic of the study in the field of immunology. Both DAMPs and Pathogen-associated molecular patterns (PAMPs) initiate and perpetuate the inflammatory responses via the same pattern recognition receptors (PRRs), with DAMPs being involved in non-infectious, and PAMPs in infectious responses.
Our group recognized that seriously injured trauma patients develop sepsis-like syndrome, while no bacteria were detected in the body. We hypothesized that mitochondria (originating from saprophytic bacteria) damaged and released from the injured tissues may contain molecules that are recognized by the immuneologic system as “foreign” and therefore induce a strong immune response, similar to sepsis. Indeed, we detected high levels of mitochondrial DNA (mtDNA) in blood of seriously injured blunt trauma patients. Further, we confirmed in in vitro studies that mtDNA and damaged mitochondria induce strong immune responses in neutrophils. Moreover, administration of damaged mitochondria induced Systemic Inflammatory Response Ssyndrome (SIRS) in animals. These data/observations initiated many interesting studies on the mtDAMPs. Some described mtDAMPs association with HMGB-1. There are still fewer members that constitute DAMPs compared to PAMPs. Other molecules, including HMGB-1, S-100, HSP 30/60, ATP, and B7-H3 were also recognized as DAMPs. These are very important molecules that regulate immune responses and dysregulation of these molecules will lead to various diseases.
We are inviting papers from authors interested in basic or clinical studies related to mtDAMPs, mtDNA and/or mitochondrial proteins. Any mechanistic work showing how mtDAMPs released from the sites of injury migrate into circulation may enrich the field.
We are also looking for new findings presenting combined effects of mtDAMPs with other known DAMPs, such as ATP, HMGB1, S100, and heat shock proteins. We welcome basic research, clinical research and review articles focused on mitochondrial DAMPs.
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