Tissue inflammation is a complex concerted multiphase response, mainly mediated by the immune system, as a consequence of an injury or to fight infection. Short term and moderate inflammation is necessary to heal damaged tissues and get rid of invading micro-organisms. On the contrary, long-lasting, also known as “chronic”, or intense acute inflammation are typical of the so-called “inflammatory diseases” but they also constitute the background of pathological conditions only recently attributed to an abnormal inflammatory state. Among these diseases representing a major global health burden worldwide, are now included stroke, atherosclerosis, neurological syndromes, etc.
It gains momentum that extracellular nucleotides (ATP, ADP, UTP, UDP, etc.) and nucleosides (mainly adenosine), can mediate both pro- or anti-inflammatory responses once released from damaged tissues or as a consequence of non-self interaction (i.e. by micro-organisms, parasites, allergens, tissue antigens).
Nucleosides and nucleotides are mainly synthesized intracellularly but they are also released and transformed extracellularly by membrane channels and transporters. Before their degradation by plasma membrane or soluble ectonucleotidases (CD39 and CD73), nucleotide and nucleosides bind to specific plasma membrane receptors named P2 and P1 purinergic receptors and module almost all known biologic functions. Among them, production of cytokines, chemokines and inflammatory mediators such as reactive oxygen intermediates and granular enzymes.
This Research Topic will describe the most recent acquisitions on the role of extracellular nucleotides and nucleosides as powerful modulators of the immune responses involved in the physiological defense response as well as in the pathological background of several diseases. We will also refer to pharmacological intervention on purinergic signaling to block at different levels, excessive and/or inappropriate immune responses involved in illnesses, with the goal of favoring the resolution pathways. A comprehensive overview of the biochemical, immunological and pharmacological significance of purinergic signaling in inflammation and immunity will be given. Therefore, we welcome the submission of Original Research, Brief Report, Review, Mini-Review, and Perspective articles focusing on, but not limited to, the following topics:
· Autoimmune Diseases and Purinergic-mediated Inflammation.
· Brain Diseases and Purinergic Signaling.
· Cancer, Purinergic Signaling and Inflammation.
· Gut Inflammation: How to Control it by Modulating the Purinergic Signaling.
· Airways Inflammation and Purinergic Signaling.
· Pain, a Matter of Purinergic Signaling.
· Pharmacological Targeting of Purinergic Signaling to Control Inflammation
· Skin Inflammation and Purinergic Signaling.
· Transplantation and Purinergic Signaling.
Tissue inflammation is a complex concerted multiphase response, mainly mediated by the immune system, as a consequence of an injury or to fight infection. Short term and moderate inflammation is necessary to heal damaged tissues and get rid of invading micro-organisms. On the contrary, long-lasting, also known as “chronic”, or intense acute inflammation are typical of the so-called “inflammatory diseases” but they also constitute the background of pathological conditions only recently attributed to an abnormal inflammatory state. Among these diseases representing a major global health burden worldwide, are now included stroke, atherosclerosis, neurological syndromes, etc.
It gains momentum that extracellular nucleotides (ATP, ADP, UTP, UDP, etc.) and nucleosides (mainly adenosine), can mediate both pro- or anti-inflammatory responses once released from damaged tissues or as a consequence of non-self interaction (i.e. by micro-organisms, parasites, allergens, tissue antigens).
Nucleosides and nucleotides are mainly synthesized intracellularly but they are also released and transformed extracellularly by membrane channels and transporters. Before their degradation by plasma membrane or soluble ectonucleotidases (CD39 and CD73), nucleotide and nucleosides bind to specific plasma membrane receptors named P2 and P1 purinergic receptors and module almost all known biologic functions. Among them, production of cytokines, chemokines and inflammatory mediators such as reactive oxygen intermediates and granular enzymes.
This Research Topic will describe the most recent acquisitions on the role of extracellular nucleotides and nucleosides as powerful modulators of the immune responses involved in the physiological defense response as well as in the pathological background of several diseases. We will also refer to pharmacological intervention on purinergic signaling to block at different levels, excessive and/or inappropriate immune responses involved in illnesses, with the goal of favoring the resolution pathways. A comprehensive overview of the biochemical, immunological and pharmacological significance of purinergic signaling in inflammation and immunity will be given. Therefore, we welcome the submission of Original Research, Brief Report, Review, Mini-Review, and Perspective articles focusing on, but not limited to, the following topics:
· Autoimmune Diseases and Purinergic-mediated Inflammation.
· Brain Diseases and Purinergic Signaling.
· Cancer, Purinergic Signaling and Inflammation.
· Gut Inflammation: How to Control it by Modulating the Purinergic Signaling.
· Airways Inflammation and Purinergic Signaling.
· Pain, a Matter of Purinergic Signaling.
· Pharmacological Targeting of Purinergic Signaling to Control Inflammation
· Skin Inflammation and Purinergic Signaling.
· Transplantation and Purinergic Signaling.