Molecular Signaling Pathways in Acute and Chronic Inflammation and Pain

Dear Colleagues,

Emerging research indicates that nociceptor neurons may have a significant impact on the immune response and inflammation. This suggests that pain is not only a prominent feature of inflammation but that it also plays a crucial role in regulating the immune system. When exposed to noxious stimuli, nociceptors can release neuropeptides and neurotransmitters that exert potent regulatory effects on the vasculature, as well as on innate and adaptive immunity. Various immune cells, including dendritic cells, neutrophils, macrophages, mast cells, and T cells, possess receptors for these neuronal mediators, enabling direct responses to nociceptors. It is increasingly evident that interactions between nociceptor neurons and the immune system are pivotal in both pain perception and inflammation. The dysregulation of these interactions could potentially underlie the development of inflammatory conditions affecting the skin, joints, respiratory system, and gastrointestinal tract. Furthermore, these neuroimmune interactions have been observed in peripheral tissues of damage as well as in the central nervous system. Understanding the interplay between nociceptors, immune cells, and glial cells can aid in the discovery of novel mechanisms underlying inflammatory disorders, and in the development of innovative therapeutics to treat and prevent inflammatory diseases and chronic pain. While several molecules may contribute to the onset of acute and chronic inflammation and pain, their precise mechanisms have not yet been elucidated. More recently, our understanding of the molecular mechanisms initiating the resolution of inflammation and pain has opened up new avenues for strategies aimed at managing complex acute and chronic inflammatory diseases and pain. However, it is important to note that resolution pathways are diverse and likely vary depending on the specific tissue and stimulus involved.

In the context of this Special Issue, we welcome submissions of original research and reviews pertaining to acute and chronic inflammation as well as pain. We specifically encourage contributions that emphasize the molecular mechanisms underlying the persistence of inflammation and pain, in contrast to their resolution.

Dr. Ping-Heng Tan
Guest Editor

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• inflammation
• pain
• immune response
• nervous system
• molecular mechanism