Resolution of Inflammation: Leukocytes and Molecular Pathways as Potential Therapeutic Targets

trafficking also modulates neutrophil apoptosis, another control point in resolving inflammation.Data emerging from a variety of experimental models demonstrated that resolvins and protectins limit adaptive immunity in asthma, attenuate adipose tissue inflammation and metabolic dysfunctions, including type-2 diabetes mellitus-associated insulin resistance and non-alcoholic fatty acid liver disease, and protect the kidney against diabetic nephropathy.The glucocorticoid-regulated protein annexin A1 may act in concert with lipoxins to limit inflammation underlying myocardial ischemia/reperfusion, arthritis, multiple sclerosis, and sepsis.Altering local adenosine signaling affects leukocyte activation and trafficking, and may restore tissue homeostasis in liver injury and rheumatoid arthritis.The nuclear proteins proliferating cell nuclear antigen (PCNA) and myeloid nuclear differentiation antigen (MNDA) play opposing roles in modulating neutrophil apoptosis in patient with sepsis.Targeting the complement C5a receptors C5Ra and C5L2 may attenuate excessive inflammation in sepsis and autoimmune diseases.Intracellular molecular mechanisms have also been implicated in dampening inflammation.The NOD-like receptors NOD1 and NOD2 recognize intracellular pathogens and activate transcriptional responses that would lead to restriction of infection.Suppression of IFNγ production in T lymphocytes by allopurinol may attenuate cell-mediated inflammatory diseases.This Research Topic focuses on articles that discuss the molecular mechanisms governing the function and fate of leukocytes during inflammation and identify potential targets for development of innovative therapeutic approaches for the treatment of inflammatory pathologies based on mimicking and/or activating endogenous pro-resolution mechanisms.