As critical mediators of the local and systemic inflammatory response, cytokines (e.g., IL-1, TNF, and IL-6) are produced following any inflammation. The inflammation process is the immune systems' protective response to an injurious stimulus (e.g., infections, antibodies, or physical injuries). Autoregulation is an intrinsic property and a key modulator of inflammatory response. Many investigators have provided insights into some aspects of the autoregulatory mechanism, but many critical components remain unknown. One of the autoregulatory mechanisms is the regulatory role of neurons and glial cells in inflammation and autoreceptors. A presynaptic receptor, including autoreceptor and heteroreceptor, is a receptor that, when bound by ligand, reduces the release of that ligand into the synapse and mediates the inhibition of other neurotransmitters in addition to its own ligand synthesis and release. For instance, presynaptic serotonin (5-HT) inhibitory autoreceptors reduce 5-HT release when bound by 5-HT. Some endogenous mediators and some neurotransmitters such as histamine, serotonin, acetylcholine themselves are key regulators of inflammation transition and have autoregulatory negative feedback or positive feedback to maintain cytokine release from inflammation sites.
Many receptors appear to modulate neurotransmitter release through excitatory or inhibitory mechanisms. Presynaptic receptors or autoreceptors provide a feedback mechanism on transmitter release. We are looking to receive manuscripts that show autoreceptors such as serotonin, adrenergic, endogenous opioids, nitric oxide, neurokinins, cannabinoid, GABAB, nicotinic receptors, oxytocin, vasopressin, etc. that play critical roles in self-limiting the activation process. Given that the action of some of these autoreceptors in the inflammation response is not clear, data should implicate the main autoreceptors as a key "molecular switch" that allows inflammatory molecular responses to self-limit their activation state. We propose that therapeutics targeting these autoregulatory pathways may represent new ways to treat the inflammatory response.
We welcome submissions relating but not limited to the following areas:
· Autoregulatory mechanisms in the inflammatory response.
· Serotonin, adrenergic, endogenous opioids, nitric oxide, neurokinins, acetylcholine, vasopressin, cannabinoid autoreceptors that play critical roles in self-limiting of the inflammation process.
· The importance of autoreceptors in induction or maintenance of inflammation in animal models of sepsis, spinal cord injury, airway smooth muscle obstruction, and other related inflammatory conditions.
· Autoreceptor systems that exhibit autoregulation through autocrine activation of autoreceptors and paracrine activation of receptors on presynaptic terminals or even have a secretory response in physiological or pathophysiological disorders.
· Negative feedback receptors that are involved non-exclusively in the regulation of synthesis and vesicular release of transmitter, but also in the activation of its reuptake.
As critical mediators of the local and systemic inflammatory response, cytokines (e.g., IL-1, TNF, and IL-6) are produced following any inflammation. The inflammation process is the immune systems' protective response to an injurious stimulus (e.g., infections, antibodies, or physical injuries). Autoregulation is an intrinsic property and a key modulator of inflammatory response. Many investigators have provided insights into some aspects of the autoregulatory mechanism, but many critical components remain unknown. One of the autoregulatory mechanisms is the regulatory role of neurons and glial cells in inflammation and autoreceptors. A presynaptic receptor, including autoreceptor and heteroreceptor, is a receptor that, when bound by ligand, reduces the release of that ligand into the synapse and mediates the inhibition of other neurotransmitters in addition to its own ligand synthesis and release. For instance, presynaptic serotonin (5-HT) inhibitory autoreceptors reduce 5-HT release when bound by 5-HT. Some endogenous mediators and some neurotransmitters such as histamine, serotonin, acetylcholine themselves are key regulators of inflammation transition and have autoregulatory negative feedback or positive feedback to maintain cytokine release from inflammation sites.
Many receptors appear to modulate neurotransmitter release through excitatory or inhibitory mechanisms. Presynaptic receptors or autoreceptors provide a feedback mechanism on transmitter release. We are looking to receive manuscripts that show autoreceptors such as serotonin, adrenergic, endogenous opioids, nitric oxide, neurokinins, cannabinoid, GABAB, nicotinic receptors, oxytocin, vasopressin, etc. that play critical roles in self-limiting the activation process. Given that the action of some of these autoreceptors in the inflammation response is not clear, data should implicate the main autoreceptors as a key "molecular switch" that allows inflammatory molecular responses to self-limit their activation state. We propose that therapeutics targeting these autoregulatory pathways may represent new ways to treat the inflammatory response.
We welcome submissions relating but not limited to the following areas:
· Autoregulatory mechanisms in the inflammatory response.
· Serotonin, adrenergic, endogenous opioids, nitric oxide, neurokinins, acetylcholine, vasopressin, cannabinoid autoreceptors that play critical roles in self-limiting of the inflammation process.
· The importance of autoreceptors in induction or maintenance of inflammation in animal models of sepsis, spinal cord injury, airway smooth muscle obstruction, and other related inflammatory conditions.
· Autoreceptor systems that exhibit autoregulation through autocrine activation of autoreceptors and paracrine activation of receptors on presynaptic terminals or even have a secretory response in physiological or pathophysiological disorders.
· Negative feedback receptors that are involved non-exclusively in the regulation of synthesis and vesicular release of transmitter, but also in the activation of its reuptake.