TABLE 1.
Damage-associated molecular patterns (DAMPs): physiological activities and pathological activities during traumatic hemorrhagic shock.
| Molecule | Normal cellular activity | Actions as DAMPs |
|---|---|---|
| Syndecans | -Core proteins in the glycocalyx network (Reitsma et al., 2007) | -Degradation of syndecans promotes inflammation and leukocyte tissue migration (Reitsma et al., 2007; Wang et al., 2014) |
| -Enzymatic interactions (Reitsma et al., 2007) | -Syndecan-1 level ≥40 ng/ml is a sign of unfavorable outcome (Wang et al., 2014) | |
| -Keeping platelets and leukocytes towards the center of the vessels (Reitsma et al., 2007) | ||
| HMGB1 (High-Mobility Group Box 1) | -Nucleic protein | -Release of cytokines (Bandyopadhyay et al., 2007; Skelton and Purcell, 2020) |
| -Protein–DNA binding, transcription, replication, and DNA repair (Bianchi and Agresti, 2005) | -Activation of leukocytes, platelets, and endothelial cells (Tang et al., 2012) | |
| -Stimulation of platelet aggregation and thrombus formation (Pérez-Casal et al., 2005) | ||
| -Coagulation disturbances: PAI-1, thrombomodulin, tPA, and INR (Cohen et al., 2009) | ||
| S100 proteins | -Fight against infection, cell division, inflammation, apoptosis, and energy metabolism (Relja and Land, 2020) | -Stimulation of the secretion of E-selectin and vWF by activated endothelial cells (Ueno H, et al., 2004) |
| -Increase of apoptotic endothelial cells in vivo (Relja and Land, 2020) | ||
| -Increase of vascular permeability (Fiuza C, et al., 2003) | ||
| Nucleic acids | -Nuclear DNA, RNA, and mitochondrial DNA | -Release of pro-inflammatory cytokines (Dang et al., 2014; Pottecher et al., 2019) |
| -Neutrophil extracellular traps (NETs) (Papayannopoulos and Zychlinsky, 2009) | ||
| -Activation of proteases of the cascade coagulation (Shibamiya A, et al., 2007) | ||
| Histones | -Nucleosomes | -Endothelial cell toxicity (Viemann et al., 2005; Xu et al., 2009) |
| -Inhibition of protein C activation (Viemann et al., 2005; Xu et al., 2009) | ||
| -Microthrombi (Viemann et al., 2005; Xu et al., 2009) | ||
| -Increase of thrombin–antithrombin complex (TAT) (Viemann et al., 2005) | ||
| Extracellular vesicles | -Same composition as membrane of their cellular origin (Liaw PC, et al., 2016) | -Promotion of a procoagulant state of the endothelium (Kannemeier C, et al., 2007) |
| -Containing intracellular components (György et al., 2011) | ||
| Heat shock proteins (HSP) | -Chaperones for other molecules | -High levels of HSP70 in severe trauma patients (Chabert, 2017) |
| -Fight against stresses, including hypo and hyperthermia, UV radiation, and pathogens (Chabert, 2017) | -Ligand of TLR4 (Toll-like receptor) (Chabert, 2017) | |
| -Correlation between HSP60 and development of acute lung injury after trauma (Kim and Yenari, 2013) |
Shown are examples of some molecules known to have DAMP, activity during traumatic hemorrhagic shock. All of these molecules have physiological activities in the absence of trauma. Faced with an attack on the body, high levels of DAMPs, can modify the pro- or anti-inflammatory balance of the systemic response.