IL-10 and CXCL2 in trigeminal ganglia in neuropathic pain

Iwasa, Takuma; Afroz, Shaista; Inoue, Miho; Arakaki, Rieko; Oshima, Masamitsu; Raju, Resmi; Waskitho, Arief; Inoue, Masahisa; Baba, Otto; Matsuka, Yoshizo

doi:10.1016/j.neulet.2019.03.031

Cited by 32 publications

(25 citation statements)

References 46 publications

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“…44 In an animal model of trigeminal neuralgia, recombinant IL-10 treatment reduced pain by suppressing a neuronal pain mediator, CXCL-2, expression in trigeminal ganglia. 51 These studies are in support of our data that systemic IL-10 administration can effectively reduce neurogenic proinflammatory mediators in sensory neurons and painful symptoms.…”

supporting

confidence: 79%

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Yanik¹,

Dauch²,

Cheng³

2020

JPR

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supporting

confidence: 79%

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Yanik¹,

Dauch²,

Cheng³

2020

JPR

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“…Similarly, reduction of pro-inflammatory cytokine signaling by using inhibitors of TNFα, IL-1β, and IL-6 receptors have been shown to attenuate neuronal hypersensitivity after nerve-injury [25,26,27]. Other approaches to target proinflammatory cytokines include intrathecal administration of adeno-associated viral (AAV) vectors that encode the anti-inflammatory cytokine IL-10, or direct injection of recombinant IL-10 into the trigeminal ganglion, which were both found to alleviate neuropathic pain in animal models [28,29].…”

Section: Therapies Targeting Peripheral Nociceptive Circuit Dysfunmentioning

confidence: 99%

Pathological Mechanisms and Therapeutic Targets for Trigeminal Neuropathic Pain

Bista

Imlach

2019

Medicines

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Trigeminal neuropathic pain is a chronic pain condition caused by damage or inflammation of the trigeminal nerve or its branches, with both peripheral and central nervous system dysfunction contributing to the disorder. Trigeminal pain conditions present with diagnostic and therapeutic challenges to healthcare providers and often require multiple therapeutic approaches for pain reduction. This review will provide the overview of pathophysiology in peripheral and central nociceptive circuits that are involved in neuropathic pain conditions involving the trigeminal nerve and the current therapeutics that are used to treat these disorders. Recent advances in treatment of trigeminal pain, including novel therapeutics that target ion channels and receptors, gene therapy and monoclonal antibodies that have shown great promise in preclinical studies and clinical trials will also be described.

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“…In addition, other studies have demonstrated SGC proliferation and activation in the TG following chronic constriction injury of the infraorbital nerve (Donegan, Kernisant, Cua, Jasmin, & Ohara, 2013; Iwasa et al, 2019). Our study also observed GFAP‐positive SGCs wrapped with primary sensory neurons in the TG.…”

Section: Discussionmentioning

confidence: 95%

Brain‐derived neurotrophic factor and Glial cell line‐derived neurotrophic factor expressions in the trigeminal root entry zone and trigeminal ganglion neurons of a trigeminal neuralgia rat model

Luo

Lin

et al. 2020

The Anatomical Record

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Microvascular compression on the trigeminal root entry zone (TREZ) is the main etiology of trigeminal neuralgia (TN) patients. To investigate brainderived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) in the trigeminal ganglion (TG) and TREZ, immunofluorescence staining and Western blot were used in a rat TN model. Both BDNF and GDNF were observed in the TG neurons and TREZ. The expression of the BDNF dimer in the TG was increased in the TN group, while GDNF expression was decreased after compression injury. The BDNF dimer/pro-BDNF ratio in the TREZ of the TN group was higher than that in the sham group, but the GDNF expression in the TREZ was significantly lower than that in the sham group. These results suggested that compression injury in the TREZ of rats induced dynamic changes in BDNF and GDNF in both the TG and TREZ, and these changes are involved in the nociceptive transmission of the TN animal model. K E Y W O R D S brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, trigeminal neuralgia, animal model, trigeminal root entry zone, trigeminal ganglion, chronic compression 1 | INTRODUCTION Trigeminal neuralgia (TN) is one of the most severe orofacial neuropathic pain conditions affecting patients. While accumulating evidence has indicated that aberrant neurovascular compression on the trigeminal root entry zone (TREZ) is the main etiology of TN (Cruccu et al., 2016), its pathogenesis remains unknown. The trigeminal ganglion (TG) is the peripheral ganglion of the trigeminal sensory pathway, which contains different sensory neurons and satellite glial cells (SGCs). Neurons in the TG respond to innocuous and noxious stimuli from the orofacial area. Interestingly, neurons in the TG have no dendrites, but several SGCs wrap each neuron to form a completed glial sheath, which is a unique morphological and, most likely, functional unit (Hanani, 2005). Brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) are two important Abbreviations: BDNF, brain-derived neurotrophic factor; CCT, chronic compression of the trigeminal root; CNS, central nervous system; GDNF, glial cell line-derived neurotrophic factor; POD, postoperation day; PNS, peripheral nervous system; SGCs, satellite glial cells; TG, trigeminal ganglion; TN, trigeminal neuralgia; TREZ, trigeminal root entry zone. Daoshu Luo and Lili Luo contributed equally to this study.

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IL-10 and CXCL2 in trigeminal ganglia in neuropathic pain

Cited by 32 publications

References 46 publications

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Pathological Mechanisms and Therapeutic Targets for Trigeminal Neuropathic Pain

Brain‐derived neurotrophic factor and Glial cell line‐derived neurotrophic factor expressions in the trigeminal root entry zone and trigeminal ganglion neurons of a trigeminal neuralgia rat model

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