Modulatory effect of botulinum toxin type A on the microglial P2X7/CatS/FKN activated-pathway in antigen-induced arthritis of the temporomandibular joint of rats

Muñoz-Lora, Victor Ricardo Manuel; Abdalla, Henrique Ballassini; Cury, Altair Antoninha Del Bel; Clemente‐Napimoga, Juliana Trindade

doi:10.1016/j.toxicon.2020.08.027

Cited by 21 publications

(22 citation statements)

References 30 publications

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“…These results were validated in a separate study by the same group using a similar model of TMJ arthritis induced by CFA and methylated BSA (35). As expected, P2X7, FKN, and CatS levels were elevated in the trigeminal Vc.…”

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painsupporting

confidence: 77%

“…The results indicate that in this model the FKN/CX3CR1 axis does not act as a pronociceptive factor at the trigeminal level in STZ rats (36). The contrasting findings from this model (showing increases in FKN/CX3CR1 with reduced nociceptive behaviour) compared to others (showing increases in expression of FKN/CX3CR1 linked with increased nociceptive responses) (34,35) illustrates the complexity of nociceptive mechanisms in different pain conditions and indicates variability between different pain models. Interestingly, contrasting evidence from studies in the spinal system of STZ mice indicates that FKN/CX3CR1 could participate as a pronociceptive factor, as shown by paw withdrawal thresholds measured in KO and WT CX3CR1 STZ mice (77).…”

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 72%

“…The chemokine response could be reversed by treatment with botulinum toxin type A (BoNT/A). In this study, microglial activation was not assessed; however, the authors propose that BoNT/A could be reducing P2X7 expression and therefore inhibiting the microglia-neuron crosstalk through CatS and FKN (35).…”

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 94%

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Chemokines and Pain in the Trigeminal System

2021

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Chemotactic cytokines or chemokines are a large family of secreted proteins able to induce chemotaxis. Chemokines are categorized according to their primary amino acid sequence, and in particular their cysteine residues that form disulphide bonds to maintain the structure: CC, CXC, CX3C, and XC, in which X represents variable amino acids. Among their many roles, chemokines are known to be key players in pain modulation in the peripheral and central nervous systems. Thus, they are promising candidates for novel therapeutics that could replace current, often ineffective treatments. The spinal and trigeminal systems are intrinsically different beyond their anatomical location, and it has been suggested that there are also differences in their sensory mechanisms. Hence, understanding the different mechanisms involved in pain modulation for each system could aid in developing appropriate pharmacological alternatives. Here, we aim to describe the current landscape of chemokines that have been studied specifically with regard to trigeminal pain. Searching PubMed and Google Scholar, we identified 30 reports describing chemokines in animal models of trigeminal pain, and 15 reports describing chemokines involved in human pain associated with the trigeminal system. This review highlights the chemokines studied to date at different levels of the trigeminal system, their cellular localization and, where available, their role in a variety of animal pain models.

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Section: Other Evidence Of Chemokine Activation In Animal Models Of Painsupporting

confidence: 77%

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 72%

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 94%

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Chemokines and Pain in the Trigeminal System

2021

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“…Whereas CFA is typically used for modeling tonic/chronic pain, other pro-inflammatory agents, such as carrageenan, zymosan, capsaicin, and formalin, are used to model acute TMJ pain. Similar to CFA, carrageenan, zymosan, capsaicin, or formalin injections in the TMJ increase the expression of the microglial markers Iba1 and CD11b in the TNC [35,37,38,101]. Capsaicin and formalin injections into the TMJ induce increased p38 phosphorylation in microglia in the TNC and expression of connexin 26, 36, and 40 in SGCs in the TG [37,38,102].…”

Section: Glial Cells Activation In Other Animal Models Of Tmdmentioning

confidence: 98%

Glia and Orofacial Pain: Progress and Future Directions

Salvo

Akerman

et al. 2021

IJMS

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Orofacial pain is a universal predicament, afflicting millions of individuals worldwide. Research on the molecular mechanisms of orofacial pain has predominately focused on the role of neurons underlying nociception. However, aside from neural mechanisms, non-neuronal cells, such as Schwann cells and satellite ganglion cells in the peripheral nervous system, and microglia and astrocytes in the central nervous system, are important players in both peripheral and central processing of pain in the orofacial region. This review highlights recent molecular and cellular findings of the glia involvement and glia–neuron interactions in four common orofacial pain conditions such as headache, dental pulp injury, temporomandibular joint dysfunction/inflammation, and head and neck cancer. We will discuss the remaining questions and future directions on glial involvement in these four orofacial pain conditions.

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“…Most studies suggest that BTX-A exerts its analgesic effects by releasing certain transmitters in the peripheral nervous system (such as calcitonin gene-related peptides, substance P and glutamate), anti-inflammatory and other modulation the peripheral nervous system (W.C. Lee et al, 2018;Muñoz-Lora et al, 2020;She et al, 2020). On the other hand, BTX-A exerts its therapeutic effect on pain by activating glial cells such as microglia and astrocytes and regulating the central nervous system-related pathways such as the upstream pain transmission pathway (Shi et al, 2019;Valois et al, 2020).…”

Section: Figure 1 Outline Of the Mechanism Of Btx-a In Treating Painmentioning

confidence: 99%

Advances in botulinum toxin type A for the treatment of pain

Jiang¹,

Huang²,

Yang³

et al. 2021

NRFHH

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<i>Clostridium botulinum</i> (CB) is a Gram-positive anaerobic bacterium and a significant cause of food spoilage. Foodborne botulism occurs worldwide every year and even lead to death from respiratory distress in severe cases after eating botulism-contaminated food. The pathogenicity of CB lies in its ability to produce a potent neurotoxin, “botulinum toxin (BTX)”, for which eight different subtypes have already been isolated so far. Botulinum toxin type A (BTX-A) is widely used to treat critical clinical issues due to its good affinity and tolerability. Studies have shown that BTX-A injections effectively treat myofascial pain, inflammatory pain, and neuropathic pain. The current article mainly reviews the latest research progress using BTX-A in pain treatment during two years.

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Modulatory effect of botulinum toxin type A on the microglial P2X7/CatS/FKN activated-pathway in antigen-induced arthritis of the temporomandibular joint of rats

Cited by 21 publications

References 30 publications

Chemokines and Pain in the Trigeminal System

Chemokines and Pain in the Trigeminal System

Glia and Orofacial Pain: Progress and Future Directions

Advances in botulinum toxin type A for the treatment of pain

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