Inflammation is a major mechanism that allows the immune system to inactivate and clear invading microorganisms. Recently, the so called sterile inflammation has also been shown to be activated by endogenous components, termed danger-associated molecular patterns (DAMPs) that are released whenever cell damage occurs. Thus, inflammation is increasingly recognized as an important component of virtually any chronic condition, from neurodegenerative, cardiovascular, metabolic, respiratory, renal, digestive and musculoskeletal diseases to cancer. Moreover, inflammation is now known to be also involved in cell senescence and organismal aging. The characteristics of the inflammatory response that accompanies these diseases and conditions are, nonetheless, quite distinct from those that occur in acute responses to microbial invaders and in autoimmune diseases. Instead of the massive invasion of the affected tissue by neutrophils, monocytes and lymphocytes, that characterizes acute inflammation, in chronic conditions leukocyte infiltration is much less marked or even absent. Nonetheless, there is always a significant increase in the levels of pro-inflammatory factors, including cytokines (like interleukin (IL)-1? and ?, IL-6, IL-18 and TNF-?), chemokines, eicosanoids, adipokines, miokines, etc, which frequently also translates into increased plasma levels. This is particularly relevant as such agents can contribute to damage distant cells and tissues. On the other hand, those inflammatory factors can further aggravate cell and tissue damage by increasing their own synthesis and secretion in an autocrine or paracrine manner. Furthermore, recent evidence has shed light on a novel mode of intercellular communication mediated by exosomes, a class of extracellular vesicles, in regulating inflammation. The delivery of other cellular products through exosomes, namely miRNAs, can further enhance the propagation of inflammatory signals to distant cells and tissues.
Although inflammation is virtually present in any chronic disease, whether this response is the outcome of other processes that drive the disease or, instead, being itself a mechanism that promotes cell and tissue damage, is an effector of the disease process remains to be fully elucidated. Understanding the role of inflammation in each of those diseases is thus crucial to determine its value as a therapeutic target “latu sensu” and more precisely to identify specific components, from DAMPs, miRNAs, cytokines and their receptors to signaling pathways, and cellular processes whose modulation can be effective in preventing, treating and curing each of those diseases. This research topic aims at bringing together current knowledge on critical processes for cell homeostasis that are reciprocally modulated and/or impaired by inflammation and that are affected in and contribute to disease and so, welcomes original articles and focused reviews that tackle these subjects, either from a basic research or clinical point of view.
Inflammation is a major mechanism that allows the immune system to inactivate and clear invading microorganisms. Recently, the so called sterile inflammation has also been shown to be activated by endogenous components, termed danger-associated molecular patterns (DAMPs) that are released whenever cell damage occurs. Thus, inflammation is increasingly recognized as an important component of virtually any chronic condition, from neurodegenerative, cardiovascular, metabolic, respiratory, renal, digestive and musculoskeletal diseases to cancer. Moreover, inflammation is now known to be also involved in cell senescence and organismal aging. The characteristics of the inflammatory response that accompanies these diseases and conditions are, nonetheless, quite distinct from those that occur in acute responses to microbial invaders and in autoimmune diseases. Instead of the massive invasion of the affected tissue by neutrophils, monocytes and lymphocytes, that characterizes acute inflammation, in chronic conditions leukocyte infiltration is much less marked or even absent. Nonetheless, there is always a significant increase in the levels of pro-inflammatory factors, including cytokines (like interleukin (IL)-1? and ?, IL-6, IL-18 and TNF-?), chemokines, eicosanoids, adipokines, miokines, etc, which frequently also translates into increased plasma levels. This is particularly relevant as such agents can contribute to damage distant cells and tissues. On the other hand, those inflammatory factors can further aggravate cell and tissue damage by increasing their own synthesis and secretion in an autocrine or paracrine manner. Furthermore, recent evidence has shed light on a novel mode of intercellular communication mediated by exosomes, a class of extracellular vesicles, in regulating inflammation. The delivery of other cellular products through exosomes, namely miRNAs, can further enhance the propagation of inflammatory signals to distant cells and tissues.
Although inflammation is virtually present in any chronic disease, whether this response is the outcome of other processes that drive the disease or, instead, being itself a mechanism that promotes cell and tissue damage, is an effector of the disease process remains to be fully elucidated. Understanding the role of inflammation in each of those diseases is thus crucial to determine its value as a therapeutic target “latu sensu” and more precisely to identify specific components, from DAMPs, miRNAs, cytokines and their receptors to signaling pathways, and cellular processes whose modulation can be effective in preventing, treating and curing each of those diseases. This research topic aims at bringing together current knowledge on critical processes for cell homeostasis that are reciprocally modulated and/or impaired by inflammation and that are affected in and contribute to disease and so, welcomes original articles and focused reviews that tackle these subjects, either from a basic research or clinical point of view.