path(MESH:Inflammation)
Analysis of lymphoid and myeloid cell populations in the meninges (Extended Data Fig. 9d) demonstrated a significant increase in the number of macrophages upon lymphatic ablation compared to both control groups (Extended Data Fig. 9e), which might be correlated with increased amyloid-β deposition and inflammation in the meninges PubMed:30046111
Similarly, stimulation of microglia with the LXR agonist, GW3965, acts simultaneously to suppress inflammation and promote fibrillar Ab stimulated phagocytosis [47]. PubMed:21718217
Together with that re- leased by vagal nerve endings, ACh can also contribute to the cholinergic control of inflammation PubMed:28901280
α7-containing receptors are expressed in neurons and non-excitable cells in order to mediate pro-proliferative, sur- vival and anti-inflammatory signalling. PubMed:28901280
First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553
First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553
The antiaggregant TauRDΔKPP slices had ramified form of microglia with 6-7 branches on an average indicating that the microglial cells were in their normal physiologically active form and there is no sign of inflammation (Fig 3d, bars 1 and 2). PubMed:29202785
On the contrary, microglia in proaggregant TauRDΔK slices, were increased in number and were also observed with 2-3 branches on an average compared to age-matched controls and also the antiaggregant TauRDΔKPP slices (Fig. 3d, bar 3). This indicates that in the pro-aggregant TauRDΔK slices the microglia are in a reactive form, indicating that there is also enhanced inflammation PubMed:29202785
Inflammation is one of major pathological changes in AD brains and NF-kB signalling plays an important role in inflammation and oxidative stress (Tong et al. 2005). PubMed:21329555
Inflammation is one of major pathological changes in AD brains and NF-kB signalling plays an important role in inflammation and oxidative stress (Tong et al. 2005). PubMed:21329555
It revealed potent anti-histone acetyltransferase (HAT) activity and inhibited RelA acetylation via direct inhibition of HAT enzymes and consequently down-regulation ofdiverse inflammatory signaling pathways [163]. PubMed:29179999
Moreover,it reveals promising anti-inflammatory actions through suppress-ing the activation of NF-B [238–240]. PubMed:29179999
The phosphorylation of the NF-B inflamma-tory pathway in A 25-35-stimulated microglial cells was inhibited by vitamin D2 via reducing ROS and inflammatory cytokines [207] PubMed:29179999
Berberine suppressed inflammatory events occurring in several inflammation-related diseases [186,187]. PubMed:29179999
Besides, it attenuated cognitive disorders nd inflam-matory reactions in A 1-42-activated AD mice[194]. PubMed:29179999
Beneficial effects of 4-O-methylhonokinol on memory were observed by the reduction of Aaggregation in A 1-42-injected mice and memory-impaired mice with its anti-oxidative and anti-inflammatory qualities [141–143]. PubMed:29179999
Moreover, tanshinone IIA inhibited apoptosis in A 25-35-induced cells [232] and exerted anti-inflammatory activity in atherosclerosis and neuroprotective activity in cerebral ischemia/reperfusion impairment [233,234] PubMed:29179999
Retinoic acid showed anti-inflammatory qualities via suppressing the expression of the inflammatory mediators IL-6, IL-12 and TNF- [216–219] and mod-ulating NF-B signaling [220,221]. PubMed:29179999
In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790
Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790
Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790
Inflammation is a key pathological hall mark of AD [61,62], NF-κB is considered as a primary regulator of inflammatory processes [10]. PubMed:27288790
ADNP expression in lymphocytes correlates with inflammation levels (36), disease state, and autophagy (13), as well as intelligence (40). PubMed:30106381
Extracellular hemoglobin and heme are pro-oxidative, proinflammatory, and cytotoxic [10–12], and can contribute to the pathology of hemolytic diseases. PubMed:26875449
Carbon monoxide has vasodilatory, anti-proliferative, anti-inflammatory and antioxidant properties, whereas bilirubin, the product of biliverdin reductase, is an antioxidant (Baranano et al, 2002). PubMed:25307023
These concepts challenged the idea that the cytotoxic and inflammatory effects of heme were exclusively mediated by the oxidative capability of the Fe associated with the amphipathic property of the porphyrin ring. PubMed:24904418
Thus, the antioxidant, anticoagulant, anti-proliferative and vasodilating effects of the HMOX1 and biliverdin reductase systems probably compensate for the nitric oxide (NO) scavenging, vasoconstrictive, proliferative, inflammatory and pro-oxidant effects of circulating free haemoglobin, haem and haem-iron, which are discussed below (Rother et al, 2005). PubMed:25307023
There are in vitro and animal model data linking increased free Hb, heme, and iron to inflammation, 6 infection,7 platelet (PLT) activation,8,9 vasculopathy, 10 and thrombosis. PubMed:29603246
Both processes decrease the availability of NO, which normally maintains smooth muscle cell relaxation, inhibits platelet activation and aggregation, and has anti-inflammatory effects on the endothelium. PubMed:29929138
These results suggest that heme plays an essential role in kidney inflammation via regulating NLRP3-Caspase-1-IL-1b axis. PubMed:24464629
CO inhibits Hb oxidation and subsequently heme release, thus blocking heme accumulation in serum and preventing heme from exerting its inflammatory effects in the course of malaria disease (Ferreira et al., 2011). PubMed:24904418
During intravascular hemolysis the serum proteins responsible for removing heme get saturated and heme can exert its inflammatory effects. PubMed:24904418
Thus, the antioxidant, anticoagulant, anti-proliferative and vasodilating effects of the HMOX1 and biliverdin reductase systems probably compensate for the nitric oxide (NO) scavenging, vasoconstrictive, proliferative, inflammatory and pro-oxidant effects of circulating free haemoglobin, haem and haem-iron, which are discussed below (Rother et al, 2005). PubMed:25307023
Free plasma haemoglobin and haem also scavenge NO and have multiple pro-inflammatory and pro-oxidant properties that mediate many of the adverse effects of haemolysis. PubMed:25307023
More recently, we have also shown that free heme is also released during storage and may mediate further inflammation28 PubMed:26202471
Free heme is a potent trigger of lipid peroxidation and a promoter of inflammation.4–6 PubMed:26794659
Increased plasma concentrations of cell-free heme, the breakdown product of 390 hemoglobin, promote activation and inflammation of endothelial cells and enhance 391 oxidative stress and vascular permeability (22). PubMed:28314763
Free hemin is a cytotoxic molecule that mediates oxidative stress, endothelial activation, and inflammation, and it is implicated in malaria pathogenesis [40] and AKI, among others [41]. PubMed:28716864
There are in vitro and animal model data linking increased free Hb, heme, and iron to inflammation, 6 infection,7 platelet (PLT) activation,8,9 vasculopathy, 10 and thrombosis. PubMed:29603246
During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434
Administration of heme in healthy volunteers caused thrombophlebitis, demonstrating that it can cause vascular inflammation followed by vascular obstruction [18]. PubMed:29929138
In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069
In mice, this response was attenuated after administration of the TLR-4 inhibitor, TAK-242, suggesting hemin potentiates pulmonary macrophage activation and inflammation through hemin-induced TLR-4 receptor binding [27]. PubMed:30281034
Malondialdehyde (MDA) represents evidence of systemic oxidative stress and inflammation [31], and is commonly used to estimate the level of lipid peroxidation. PubMed:30324533
ADP released from haemolysed RBCs induces CD40LG release from platelets and lymphocytes, thereby contributing to the pro-inflammatory and pro-thrombotic environment (Helms et al, 2013). PubMed:25307023
Storage is known to result in increased hemolysis which in turn results in loss of NO-signaling, oxidative stress and inflammation post-transfusion. PubMed:26202471
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
These ROS then oxidize cell membrane constituents to induce cytotoxicity and promote inflammation and thrombosis. PubMed:25307023
For example, Hp 2-2 has been associated with an increased susceptibility to diabetic cardiovascular disease; uptake of Hb-Hp(1-1) complexes by CD163 receptors is reportedly faster and its binding results in increased concentrations of anti-inflammatory mediators than Hb-Hp(2-2) complexes; and the angiogenic potency of Hp 2-2 is reportedly greater than that of Hp 1-1 [18]. PubMed:24486321
We recently found that, contrary to other forms of oxidized hemoglobin, ferrylhemoglobin acts as a potent pro-inflammatory agonist in endothelial cells, leading to the up-regulation of adhesion molecules that support the recruitment of macrophages into the vessel wall.36 PubMed:20378845
For example, HbFe41 (20 mM), but not HbFe31 or HbFe21, induced cytoskeletal reorganization, inflammation and disrupted barrier integrity in endothelial cells after 8 hours of incubation with the proteins. PubMed:26974230
The circulating MPs can internalize free heme and transfer it to vascular endothelium, promoting vaso-occlusion, or amplify systemic inflammation via thrombin mediated activation of the complement system [57]. PubMed:28458720
Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351
Thus, the antioxidant, anticoagulant, anti-proliferative and vasodilating effects of the HMOX1 and biliverdin reductase systems probably compensate for the nitric oxide (NO) scavenging, vasoconstrictive, proliferative, inflammatory and pro-oxidant effects of circulating free haemoglobin, haem and haem-iron, which are discussed below (Rother et al, 2005). PubMed:25307023
Free plasma haemoglobin and haem also scavenge NO and have multiple pro-inflammatory and pro-oxidant properties that mediate many of the adverse effects of haemolysis. PubMed:25307023
Depending on the scale, rate, and site of hemolysis, the primary adverse effects triggered by free Hb are vascular dysfunction, oxidative tissue damage, and altered inflammatory response [1], PubMed:26475040
Extracellular hemoglobin and heme are pro-oxidative, proinflammatory, and cytotoxic [10–12], and can contribute to the pathology of hemolytic diseases. PubMed:26875449
Plasma hemoglobin scavenges nitric oxide and causes vasoconstriction, platelet aggregation and inflammation9,22–24. PubMed:27515135
There are in vitro and animal model data linking increased free Hb, heme, and iron to inflammation, 6 infection,7 platelet (PLT) activation,8,9 vasculopathy, 10 and thrombosis. PubMed:29603246
Our findings in the complex setting of critically ill pediatric cardiac surgery patients demonstrate that higher levels of free Hb and lower levels of haptoglobin are associated with serious postoperative clinical complications (infection, thrombosis, death), immunomodulation, and inflammation. PubMed:29603246
During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434
In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069
In fact, hemolysis or heme injection in Hx−/− mice cause increased inflammation and severe renal damage compared to wild type (WT) mice (Tolosano et al., 1999; Vinchi et al., 2008). PubMed:24904418
In conclusion, an Hx-based therapy shows beneficial effects, in that it counteracts heme-induced proinflammatory activation of macrophages and attenuates some of its pathophysiologic consequences, such as chronic inflammation, hepatic fibrosis, and apoptosis (Figure 7E). PubMed:26675351
In that study, heme was shown to specifically bind to endothelial Toll-like receptors (TLR4) and trigger a cascade of inflammatory responses, which could be attributed to oxidation and degradation of cell-free Hb [73]. PubMed:24486321
However A1AT has broader functions [26, 27], abrogating inflammation via both enzyme-inhibitory and noninhibitory mechanisms [47]. PubMed:28716864
Probably the most important Hp-mediated abrogation of Hb toxicity is stabilization of heme within the central cavity of the Hb subunits, which almost completely prevents its dissociation and subsequent free heme-mediated oxidative reactions and inflammatory responses. PubMed:24486321
Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023
Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023
Although KC and IL-1β functions were not investigated during heme-induced inflammatory effects, TNF and LTB4 were described as essential inflammatory mediators during inflammatory events induced by heme. PubMed:24904418
Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023
Although KC and IL-1β functions were not investigated during heme-induced inflammatory effects, TNF and LTB4 were described as essential inflammatory mediators during inflammatory events induced by heme. PubMed:24904418
Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023
These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629
The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629
Supplementary treatment of septic mice with purified HRG from human plasma remarkably suppressed immunothrombosis in the lungs as well as the associated inflammation. PubMed:29544683
These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629
These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629
Kidney inflammation is the major pathologic process of chronic kidney disease (CKD) and acute kidney injury (AKI) which cause significant morbidity and mortality in the general population [1]. PubMed:24464629
Kidney inflammation is the major pathologic process of chronic kidney disease (CKD) and acute kidney injury (AKI) which cause significant morbidity and mortality in the general population [1]. PubMed:24464629
Sepsis/systemic inflammation is frequently associated with disseminated intravascular coagulation (DIC) being a predictor of mortality in septic patients [84, 85]. PubMed:29956069
Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246
Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069
Analysis of lymphoid and myeloid cell populations in the meninges (Extended Data Fig. 9d) demonstrated a significant increase in the number of macrophages upon lymphatic ablation compared to both control groups (Extended Data Fig. 9e), which might be correlated with increased amyloid-β deposition and inflammation in the meninges PubMed:30046111
During acute in- flammatory processes α7 AChRs attenuate renal failure induced by ische- mia/reperfusion by inhibiting pro-inflammatory cytokine expression, and subsequently decreasing cell apoptosis [180,201]. PubMed:22040696
First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553
First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553
Inflammation, a common feature of AD, can affect ligand affinity by making the pH more acidic, which promotes hyperphosphorylation of tau and induces conforma- tional changes in Aβ that hinder its clearance. PubMed:26195256
Inflammation is one of major pathological changes in AD brains and NF-kB signalling plays an important role in inflammation and oxidative stress (Tong et al. 2005). PubMed:21329555
Inflammation is one of major pathological changes in AD brains and NF-kB signalling plays an important role in inflammation and oxidative stress (Tong et al. 2005). PubMed:21329555
In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790
Inflammation is a key pathological hall mark of AD [61,62], NF-κB is considered as a primary regulator of inflammatory processes [10]. PubMed:27288790
ADNP expression in lymphocytes correlates with inflammation levels (36), disease state, and autophagy (13), as well as intelligence (40). PubMed:30106381
Plasma hemoglobin scavenges nitric oxide and causes vasoconstriction, platelet aggregation and inflammation9,22–24. PubMed:27515135
We recently found that, contrary to other forms of oxidized hemoglobin, ferrylhemoglobin acts as a potent pro-inflammatory agonist in endothelial cells, leading to the up-regulation of adhesion molecules that support the recruitment of macrophages into the vessel wall.36 PubMed:20378845
For example, HbFe41 (20 mM), but not HbFe31 or HbFe21, induced cytoskeletal reorganization, inflammation and disrupted barrier integrity in endothelial cells after 8 hours of incubation with the proteins. PubMed:26974230
Kidney inflammation is the major pathologic process of chronic kidney disease (CKD) and acute kidney injury (AKI) which cause significant morbidity and mortality in the general population [1]. PubMed:24464629
Kidney inflammation is the major pathologic process of chronic kidney disease (CKD) and acute kidney injury (AKI) which cause significant morbidity and mortality in the general population [1]. PubMed:24464629
These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629
These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629
These results suggest that heme induced activation of NLRP3-Caspase-1-IL-1b axis is involved in kidney inflammation in mice UUO model and that heme serves as a dangerous factor participates in this process. PubMed:24464629
These results suggest that heme plays an essential role in kidney inflammation via regulating NLRP3-Caspase-1-IL-1b axis. PubMed:24464629
More recently, we have also shown that free heme is also released during storage and may mediate further inflammation28 PubMed:26202471
Free heme is a potent trigger of lipid peroxidation and a promoter of inflammation.4–6 PubMed:26794659
Free hemin is a cytotoxic molecule that mediates oxidative stress, endothelial activation, and inflammation, and it is implicated in malaria pathogenesis [40] and AKI, among others [41]. PubMed:28716864
There are in vitro and animal model data linking increased free Hb, heme, and iron to inflammation, 6 infection,7 platelet (PLT) activation,8,9 vasculopathy, 10 and thrombosis. PubMed:29603246
During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434
In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069
In that study, heme was shown to specifically bind to endothelial Toll-like receptors (TLR4) and trigger a cascade of inflammatory responses, which could be attributed to oxidation and degradation of cell-free Hb [73]. PubMed:24486321
ADP released from haemolysed RBCs induces CD40LG release from platelets and lymphocytes, thereby contributing to the pro-inflammatory and pro-thrombotic environment (Helms et al, 2013). PubMed:25307023
Storage is known to result in increased hemolysis which in turn results in loss of NO-signaling, oxidative stress and inflammation post-transfusion. PubMed:26202471
In conclusion, an Hx-based therapy shows beneficial effects, in that it counteracts heme-induced proinflammatory activation of macrophages and attenuates some of its pathophysiologic consequences, such as chronic inflammation, hepatic fibrosis, and apoptosis (Figure 7E). PubMed:26675351
Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351
There are in vitro and animal model data linking increased free Hb, heme, and iron to inflammation, 6 infection,7 platelet (PLT) activation,8,9 vasculopathy, 10 and thrombosis. PubMed:29603246
Our findings in the complex setting of critically ill pediatric cardiac surgery patients demonstrate that higher levels of free Hb and lower levels of haptoglobin are associated with serious postoperative clinical complications (infection, thrombosis, death), immunomodulation, and inflammation. PubMed:29603246
During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434
In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069
Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720
There are in vitro and animal model data linking increased free Hb, heme, and iron to inflammation, 6 infection,7 platelet (PLT) activation,8,9 vasculopathy, 10 and thrombosis. PubMed:29603246
Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246
Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069
MPs are small membrane-derived vesicles that are shed upon activation, inflammation, or cell death/damage. PubMed:29929138
Sepsis/systemic inflammation is frequently associated with disseminated intravascular coagulation (DIC) being a predictor of mortality in septic patients [84, 85]. PubMed:29956069
Malondialdehyde (MDA) represents evidence of systemic oxidative stress and inflammation [31], and is commonly used to estimate the level of lipid peroxidation. PubMed:30324533
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