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Mediators, Receptors, and Signalling Pathways in the Anti-Inflammatory and Antihyperalgesic Effects of Acupuncture.

McDonald JL, Cripps AW, Smith PK - Evid Based Complement Alternat Med (2015)

Bottom Line: A proposed model has previously hypothesized that acupuncture might downregulate proinflammatory neuropeptides, proinflammatory cytokines, and neurotrophins, modulating transient receptor potential vallinoid (TRPV1), a G-protein coupled receptor which plays a central role in allergic rhinitis.Recent research has been largely supportive of this model.Further research on the complex cross talk between receptors during inflammation is also helping to elucidate the mediators and signalling pathways activated by acupuncture.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Griffith Health Institute, Griffith Health, Griffith University, Southport, QLD 4211, Australia.

ABSTRACT
Acupuncture has been used for millennia to treat allergic diseases including both intermittent rhinitis and persistent rhinitis. Besides the research on the efficacy and safety of acupuncture treatment for allergic rhinitis, research has also investigated how acupuncture might modulate immune function to exert anti-inflammatory effects. A proposed model has previously hypothesized that acupuncture might downregulate proinflammatory neuropeptides, proinflammatory cytokines, and neurotrophins, modulating transient receptor potential vallinoid (TRPV1), a G-protein coupled receptor which plays a central role in allergic rhinitis. Recent research has been largely supportive of this model. New advances in research include the discovery of a novel cholinergic anti-inflammatory pathway activated by acupuncture. A chemokine-mediated proliferation of opioid-containing macrophages in inflamed tissues, in response to acupuncture, has also been demonstrated for the first time. Further research on the complex cross talk between receptors during inflammation is also helping to elucidate the mediators and signalling pathways activated by acupuncture.

No MeSH data available.


Related in: MedlinePlus

Proposed model for the complex cross talk between various receptors and mediators in early phase response in allergic rhinitis. 1: nerve growth factor (NGF) activates tyrosine kinase A (TrkA) receptor which in turn increases production and release of substance P (SP). Activation of TrkA receptor also initiates signalling via the PI3K/PIP3 pathway to increase expression and sensitivity of transient receptor potential vallinoid (TRPV1) receptor. 2: chemokine receptors (CCR2, CCR3, and CXCR8) sensitize TRPV1 receptor via a PLCβ/PKC pathway. 3: TRPV1 receptor increases production and release of proinflammatory neuropeptides SP and CGRP which act synergistically to promote degranulation of primed mast cells. Histamine released by mast cells activates histamine 1 receptor (H1R) producing signalling via the phospholipase A2/lipoxygenase pathway to activate TRPV1, triggering early phase allergic inflammatory response. 4: chemokine receptors are heterologously desensitized by both adenosine (A2a) receptors and opioid receptors (MOR, DOR, and KOR). 5: Substance P is inhibited by met-enkephalin via Mu opioid receptors (MOR). A2a: adenosine 2a receptor, CCR2, CCR3: CC chemokine receptors 2 & 3, CXCR8: CXC chemokine receptor 8, PLCβ: phospholipase C β, PKC: protein kinase C, NGF: nerve growth factor, TRPV1: transient receptor potential vallinoid 1, TrkA: tyrosine kinase A receptor, H1R: histamine 1 receptor, SP: substance P, CGRP: calcitonin gene-related peptide, PI3K/PIP3: phosphatidylinositol 3 kinase/phosphatidylinositol phosphate 3 pathway, PLA2/LO: phospholipase A2/lipoxygenase pathway, MOR: Mu opioid receptor, DOR: delta opioid receptor, KOR: kappa opioid receptor, and MEK: met-enkephalin.
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Related In: Results  -  Collection


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fig1: Proposed model for the complex cross talk between various receptors and mediators in early phase response in allergic rhinitis. 1: nerve growth factor (NGF) activates tyrosine kinase A (TrkA) receptor which in turn increases production and release of substance P (SP). Activation of TrkA receptor also initiates signalling via the PI3K/PIP3 pathway to increase expression and sensitivity of transient receptor potential vallinoid (TRPV1) receptor. 2: chemokine receptors (CCR2, CCR3, and CXCR8) sensitize TRPV1 receptor via a PLCβ/PKC pathway. 3: TRPV1 receptor increases production and release of proinflammatory neuropeptides SP and CGRP which act synergistically to promote degranulation of primed mast cells. Histamine released by mast cells activates histamine 1 receptor (H1R) producing signalling via the phospholipase A2/lipoxygenase pathway to activate TRPV1, triggering early phase allergic inflammatory response. 4: chemokine receptors are heterologously desensitized by both adenosine (A2a) receptors and opioid receptors (MOR, DOR, and KOR). 5: Substance P is inhibited by met-enkephalin via Mu opioid receptors (MOR). A2a: adenosine 2a receptor, CCR2, CCR3: CC chemokine receptors 2 & 3, CXCR8: CXC chemokine receptor 8, PLCβ: phospholipase C β, PKC: protein kinase C, NGF: nerve growth factor, TRPV1: transient receptor potential vallinoid 1, TrkA: tyrosine kinase A receptor, H1R: histamine 1 receptor, SP: substance P, CGRP: calcitonin gene-related peptide, PI3K/PIP3: phosphatidylinositol 3 kinase/phosphatidylinositol phosphate 3 pathway, PLA2/LO: phospholipase A2/lipoxygenase pathway, MOR: Mu opioid receptor, DOR: delta opioid receptor, KOR: kappa opioid receptor, and MEK: met-enkephalin.

Mentions: Chemokine receptors, opioid receptors and TRPV1 receptors have been reported to participate in complex cross talk, not unlike that between neuropeptides, cytokines, and neurotrophins [48] Chemokine receptors and opioid receptors can inhibit each other by a process known as heterologous desensitization [48]. Adenosine, by activating A2a receptors, can also desensitize chemokine receptors [48] (see Figure 1). Chemokine receptors sensitize TRPV1; hence, any desensitization of chemokine receptors (by adenosine or opioid receptors) would inhibit the sensitization of TRPV1 (via a phospholipase C β/protein kinase C [PLCβ/PKC] pathway) [48]. Interactions between cannabinoid receptors and opioid receptors after acupuncture have been reported. Cannabinoid receptor CB2 has been shown to participate in the EA-induced increase of opioid expression in keratinocytes in inflamed skin (in a CFA rat hind paw inflammation model) [12].


Mediators, Receptors, and Signalling Pathways in the Anti-Inflammatory and Antihyperalgesic Effects of Acupuncture.

McDonald JL, Cripps AW, Smith PK - Evid Based Complement Alternat Med (2015)

Proposed model for the complex cross talk between various receptors and mediators in early phase response in allergic rhinitis. 1: nerve growth factor (NGF) activates tyrosine kinase A (TrkA) receptor which in turn increases production and release of substance P (SP). Activation of TrkA receptor also initiates signalling via the PI3K/PIP3 pathway to increase expression and sensitivity of transient receptor potential vallinoid (TRPV1) receptor. 2: chemokine receptors (CCR2, CCR3, and CXCR8) sensitize TRPV1 receptor via a PLCβ/PKC pathway. 3: TRPV1 receptor increases production and release of proinflammatory neuropeptides SP and CGRP which act synergistically to promote degranulation of primed mast cells. Histamine released by mast cells activates histamine 1 receptor (H1R) producing signalling via the phospholipase A2/lipoxygenase pathway to activate TRPV1, triggering early phase allergic inflammatory response. 4: chemokine receptors are heterologously desensitized by both adenosine (A2a) receptors and opioid receptors (MOR, DOR, and KOR). 5: Substance P is inhibited by met-enkephalin via Mu opioid receptors (MOR). A2a: adenosine 2a receptor, CCR2, CCR3: CC chemokine receptors 2 & 3, CXCR8: CXC chemokine receptor 8, PLCβ: phospholipase C β, PKC: protein kinase C, NGF: nerve growth factor, TRPV1: transient receptor potential vallinoid 1, TrkA: tyrosine kinase A receptor, H1R: histamine 1 receptor, SP: substance P, CGRP: calcitonin gene-related peptide, PI3K/PIP3: phosphatidylinositol 3 kinase/phosphatidylinositol phosphate 3 pathway, PLA2/LO: phospholipase A2/lipoxygenase pathway, MOR: Mu opioid receptor, DOR: delta opioid receptor, KOR: kappa opioid receptor, and MEK: met-enkephalin.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4539069&req=5

fig1: Proposed model for the complex cross talk between various receptors and mediators in early phase response in allergic rhinitis. 1: nerve growth factor (NGF) activates tyrosine kinase A (TrkA) receptor which in turn increases production and release of substance P (SP). Activation of TrkA receptor also initiates signalling via the PI3K/PIP3 pathway to increase expression and sensitivity of transient receptor potential vallinoid (TRPV1) receptor. 2: chemokine receptors (CCR2, CCR3, and CXCR8) sensitize TRPV1 receptor via a PLCβ/PKC pathway. 3: TRPV1 receptor increases production and release of proinflammatory neuropeptides SP and CGRP which act synergistically to promote degranulation of primed mast cells. Histamine released by mast cells activates histamine 1 receptor (H1R) producing signalling via the phospholipase A2/lipoxygenase pathway to activate TRPV1, triggering early phase allergic inflammatory response. 4: chemokine receptors are heterologously desensitized by both adenosine (A2a) receptors and opioid receptors (MOR, DOR, and KOR). 5: Substance P is inhibited by met-enkephalin via Mu opioid receptors (MOR). A2a: adenosine 2a receptor, CCR2, CCR3: CC chemokine receptors 2 & 3, CXCR8: CXC chemokine receptor 8, PLCβ: phospholipase C β, PKC: protein kinase C, NGF: nerve growth factor, TRPV1: transient receptor potential vallinoid 1, TrkA: tyrosine kinase A receptor, H1R: histamine 1 receptor, SP: substance P, CGRP: calcitonin gene-related peptide, PI3K/PIP3: phosphatidylinositol 3 kinase/phosphatidylinositol phosphate 3 pathway, PLA2/LO: phospholipase A2/lipoxygenase pathway, MOR: Mu opioid receptor, DOR: delta opioid receptor, KOR: kappa opioid receptor, and MEK: met-enkephalin.
Mentions: Chemokine receptors, opioid receptors and TRPV1 receptors have been reported to participate in complex cross talk, not unlike that between neuropeptides, cytokines, and neurotrophins [48] Chemokine receptors and opioid receptors can inhibit each other by a process known as heterologous desensitization [48]. Adenosine, by activating A2a receptors, can also desensitize chemokine receptors [48] (see Figure 1). Chemokine receptors sensitize TRPV1; hence, any desensitization of chemokine receptors (by adenosine or opioid receptors) would inhibit the sensitization of TRPV1 (via a phospholipase C β/protein kinase C [PLCβ/PKC] pathway) [48]. Interactions between cannabinoid receptors and opioid receptors after acupuncture have been reported. Cannabinoid receptor CB2 has been shown to participate in the EA-induced increase of opioid expression in keratinocytes in inflamed skin (in a CFA rat hind paw inflammation model) [12].

Bottom Line: A proposed model has previously hypothesized that acupuncture might downregulate proinflammatory neuropeptides, proinflammatory cytokines, and neurotrophins, modulating transient receptor potential vallinoid (TRPV1), a G-protein coupled receptor which plays a central role in allergic rhinitis.Recent research has been largely supportive of this model.Further research on the complex cross talk between receptors during inflammation is also helping to elucidate the mediators and signalling pathways activated by acupuncture.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Griffith Health Institute, Griffith Health, Griffith University, Southport, QLD 4211, Australia.

ABSTRACT
Acupuncture has been used for millennia to treat allergic diseases including both intermittent rhinitis and persistent rhinitis. Besides the research on the efficacy and safety of acupuncture treatment for allergic rhinitis, research has also investigated how acupuncture might modulate immune function to exert anti-inflammatory effects. A proposed model has previously hypothesized that acupuncture might downregulate proinflammatory neuropeptides, proinflammatory cytokines, and neurotrophins, modulating transient receptor potential vallinoid (TRPV1), a G-protein coupled receptor which plays a central role in allergic rhinitis. Recent research has been largely supportive of this model. New advances in research include the discovery of a novel cholinergic anti-inflammatory pathway activated by acupuncture. A chemokine-mediated proliferation of opioid-containing macrophages in inflamed tissues, in response to acupuncture, has also been demonstrated for the first time. Further research on the complex cross talk between receptors during inflammation is also helping to elucidate the mediators and signalling pathways activated by acupuncture.

No MeSH data available.


Related in: MedlinePlus