The anti-inflammatory effects of acupuncture and their relevance to allergic rhinitis: a narrative review and proposed model

John L McDonald, Allan W Cripps, Peter K Smith, Caroline A Smith, Charlie C Xue, Brenda Golianu, John L McDonald, Allan W Cripps, Peter K Smith, Caroline A Smith, Charlie C Xue, Brenda Golianu

Abstract

Classical literature indicates that acupuncture has been used for millennia to treat numerous inflammatory conditions, including allergic rhinitis. Recent research has examined some of the mechanisms underpinning acupuncture's anti-inflammatory effects which include mediation by sympathetic and parasympathetic pathways. The hypothalamus-pituitary-adrenal (HPA) axis has been reported to mediate the antioedema effects of acupuncture, but not antihyperalgesic actions during inflammation. Other reported anti-inflammatory effects of acupuncture include an antihistamine action and downregulation of proinflammatory cytokines (such as TNF- α , IL-1 β , IL-6, and IL-10), proinflammatory neuropeptides (such as SP, CGRP, and VIP), and neurotrophins (such as NGF and BDNF) which can enhance and prolong inflammatory response. Acupuncture has been reported to suppress the expression of COX-1, COX-2, and iNOS during experimentally induced inflammation. Downregulation of the expression and sensitivity of the transient receptor potential vallinoid 1 (TRPV1) after acupuncture has been reported. In summary, acupuncture may exert anti-inflammatory effects through a complex neuro-endocrino-immunological network of actions. Many of these generic anti-inflammatory effects of acupuncture are of direct relevance to allergic rhinitis; however, more research is needed to elucidate specifically how immune mechanisms might be modulated by acupuncture in allergic rhinitis, and to this end a proposed model is offered to guide further research.

Figures

Figure 1
Figure 1
The role of transient receptor potential vallinoid 1 (TRPV1) in early-phase response in allergic rhinitis. 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. 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. 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.
Figure 2
Figure 2
Complex crosstalk between inflammatory cells, neuropeptides, neurotrophins, and cytokines in allergic rhinitis. Substance P (SP) and calcitonin gene-related peptide (CGRP) act synergistically (along with vasoactive intestinal peptide (VIP)) to promote vasodilation and plasma extravasation causing nasal congestion. SP and CGRP also activate monocytes to release proinflammatory cytokines and promote degranulation of primed mast cells contributing to early-phase allergic response. Nerve growth factor (NGF) promotes the production and release of SP and CGRP and also promotes the survival of eosinophils and mast cells hence prolonging inflammatory response. CGRP: calcitonin gene-related peptide, SP: substance P, VIP: vasoactive intestinal peptide, NKA: neurokinin A, NGF: nerve growth factor, TNF-α: tumour necrosis factor alpha, IL-1: interleukin 1, IL-4: interleukin 4, IL-6: interleukin 6, IL-10: interleukin 10. Images courtesy of Dr P. K. Smith.
Figure 3
Figure 3
Proposed model for the effects of acupuncture in mucosal inflammation. CGRP: calcitonin gene-related peptide, SP: substance P, VIP: vasoactive intestinal peptide, NGF: nerve growth factor, BDNF: brain-derived neurotrophic factor, TRPV1: transient receptor potential vallinoid 1.

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