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Inflammation and its resolution are the result of the balance between pro-inflammatory and pro-resolving factors, such as specialized pro-resolving mediators (SPMs). This balance is crucial for plaque evolution in atherosclerosis, a chronic inflammatory disease. Myeloperoxidase (MPO) has been related to oxidative stress and atherosclerosis, and MPO-oxidized low-density lipoproteins (Mox-LDLs) have specific characteristics and effects. They participate in foam cell formation and cause specific reactions when interacting with macrophages and endothelial cells. They also increase the production of intracellular reactive oxygen species (ROS) in macrophages and the resulting antioxidant response. Mox-LDLs also drive macrophage polarization. Mox-LDLs are known to be pro-inflammatory particles. However, in the presence of Mox-LDLs, endothelial cells produce resolvin D1 (RvD1), a SPM. SPMs are involved in the resolution of inflammation by stimulating efferocytosis and by reducing the adhesion and recruitment of neutrophils and monocytes. RvD1 also induces the synthesis of other SPMs. In vitro, Mox-LDLs have a dual effect by promoting RvD1 release and inducing a more anti-inflammatory phenotype macrophage, thereby having a mixed effect on inflammation. In this review, we discuss the interrelationship between MPO, Mox-LDLs, and resolvins, highlighting a new perception of the role of Mox-LDLs in atherosclerosis.

Ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), which contributes to the development of chronic kidney disease (CKD). Renal IRI combines major events, including a strong inflammatory immune response leading to extensive cell injuries, necrosis and late interstitial fibrosis. Macrophages act as key players in IRI-induced AKI by polarizing into proinflammatory M1 and anti-inflammatory M2 phenotypes. Compelling evidence exists that the stress-responsive enzyme, heme oxygenase-1 (HO-1), mediates protection against renal IRI and modulates macrophage polarization by enhancing a M2 subset. Hereafter, we review the dual effect of macrophages in the pathogenesis of IRI-induced AKI and discuss the critical role of HO-1 expressing macrophages.

Introduction: Delirium is a leading cause of hospitalization and morbidity in elderly persons. Nonconvulsive status epilepticus (NCSE) and delirium share many risk factors. We tested the hypothesis that NCSE plays an important role in delirium by performing continuous EEG (cEEG) monitoring in elderly patients with delirium of any cause., Material and Methods: Patients over 65 years old presenting with delirium in the emergency room were prospectively included and underwent either routine 20-minute EEG or cEEG within 24h after admission. Clinical, biological, and imaging characteristics, length of hospitalization, and outcome were compared between patients with possible NCSE and patients without epileptic discharges., Results: There were 32 patients in each group. Continuous EEG detected patterns compatible with NCSE in 28% and focal interictal epileptiform discharges (IEDs) in 16% of the patients. Routine EEG detected patterns compatible with NCSE in 6% and focal IEDs in 16% of the patients. History of cognitive impairment and use of antibiotics and hypernatremia were significantly associated with the presence of possible NCSE. Delirium in patients with possible NCSE was initially attributed to another cause in over 80% of the cases. Patterns compatible with NCSE were associated with a longer hospitalization stay and a higher mortality rate., Conclusion: Electroencephalographic patterns compatible with NCSE are found in 28% of elderly with delirium when cEEG monitoring is performed. No clinical or paraclinical parameter can reliably distinguish elderly patients with delirium with or without patterns compatible with NCSE in the absence of cEEG monitoring. Elderly patients with delirium and patterns compatible with NCSE have significantly higher mortality rates and longer hospital stays., (Copyright © 2014 Elsevier Inc. All rights reserved.)