Inflammation arises from a complex multiphase response, mainly mediated by the interplay between immune cells and many soluble mediators, to protect the organism from harmful stimuli such as pathogens, damaged cells, toxic compounds, or irradiation. Short term and moderate inflammation is known to benefit tissue recovery and clearance of invading micro-organisms. While, long-lasting or intense acute inflammation leads to so-called “inflammatory diseases”, with massive immune cell infiltration and persistent tissue inflammation, such as myocardial ischemia, neurological disorders and inflammatory bowel diseases.
Adenosine, a pervasive autacoid, can mediate both pro- and anti-inflammatory responses once released in response to inflammation or infections. In physiological conditions, the extracellular concentrations of adenosine are maintained at a low level as a result of rapid metabolism and uptake. Nevertheless, its levels increase during metabolic change conditions, hypoxia, tissue injury, and inflammation, regulating the immune response.
Adenosine is mainly synthesized intracellularly but it is also released and transformed extracellularly by membrane channels and transporters. Once released, adenosine can be deaminated to inosine by adenosine deaminase (ADA) or taken up directly by cells through unique nucleoside transporters (ENT1 and ENT2) and re-phosphorylated to ATP. Adenosine is known to modulate almost all known biologic functions through binds to its four specific adenosine receptors (A1, A2A, A2B, A3). In recent years, there has been increased interest in the roles of adenosine as key mediators of immune regulation following micro-organism infection and tissue inflammation. We are particularly interested in further uncovering these roles and highlighting the importance of adenosine signaling within pathophysiological processes.
In this Research Topic, we aim to bring together researchers investigating all aspects of adenosine signaling (function, transformation, transportation) and produce a comprehensive overview of the most recent acquisitions on the role of adenosine as powerful modulators of the immune regulation involved in infection and inflammation. Therefore, we welcome the submission of Review, Original Research, Brief Research Report, and Perspective articles covering, but not limited to the following topics:
• autoimmune diseases and adenosine-mediated inflammation
• neurological diseases and adenosine signaling
• cardiovascular diseases and adenosine signaling
• adenosine signaling in controlling gut inflammation
• adenosine signaling in kidney diseases
• lung inflammation and adenosine signaling
• skin inflammation and adenosine signaling
• adenosine signaling in infectious diseases
• pharmacological targeting of adenosine signaling to control inflammation.
Inflammation arises from a complex multiphase response, mainly mediated by the interplay between immune cells and many soluble mediators, to protect the organism from harmful stimuli such as pathogens, damaged cells, toxic compounds, or irradiation. Short term and moderate inflammation is known to benefit tissue recovery and clearance of invading micro-organisms. While, long-lasting or intense acute inflammation leads to so-called “inflammatory diseases”, with massive immune cell infiltration and persistent tissue inflammation, such as myocardial ischemia, neurological disorders and inflammatory bowel diseases.
Adenosine, a pervasive autacoid, can mediate both pro- and anti-inflammatory responses once released in response to inflammation or infections. In physiological conditions, the extracellular concentrations of adenosine are maintained at a low level as a result of rapid metabolism and uptake. Nevertheless, its levels increase during metabolic change conditions, hypoxia, tissue injury, and inflammation, regulating the immune response.
Adenosine is mainly synthesized intracellularly but it is also released and transformed extracellularly by membrane channels and transporters. Once released, adenosine can be deaminated to inosine by adenosine deaminase (ADA) or taken up directly by cells through unique nucleoside transporters (ENT1 and ENT2) and re-phosphorylated to ATP. Adenosine is known to modulate almost all known biologic functions through binds to its four specific adenosine receptors (A1, A2A, A2B, A3). In recent years, there has been increased interest in the roles of adenosine as key mediators of immune regulation following micro-organism infection and tissue inflammation. We are particularly interested in further uncovering these roles and highlighting the importance of adenosine signaling within pathophysiological processes.
In this Research Topic, we aim to bring together researchers investigating all aspects of adenosine signaling (function, transformation, transportation) and produce a comprehensive overview of the most recent acquisitions on the role of adenosine as powerful modulators of the immune regulation involved in infection and inflammation. Therefore, we welcome the submission of Review, Original Research, Brief Research Report, and Perspective articles covering, but not limited to the following topics:
• autoimmune diseases and adenosine-mediated inflammation
• neurological diseases and adenosine signaling
• cardiovascular diseases and adenosine signaling
• adenosine signaling in controlling gut inflammation
• adenosine signaling in kidney diseases
• lung inflammation and adenosine signaling
• skin inflammation and adenosine signaling
• adenosine signaling in infectious diseases
• pharmacological targeting of adenosine signaling to control inflammation.
