CXCL10 and CXCR3 in the Trigeminal Ganglion Contribute to Trigeminal Neuropathic Pain in Mice

Ju, Yuanyuan; Jiang, Ming; Xu, Feifei; Wang, Dongqin; Ding, Bi-Xiao; Ma, Lingjie; Wu, Hao

doi:10.2147/jpr.s288292

Cited by 20 publications

(28 citation statements)

References 47 publications

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“…A recent study supports a direct link between the CXCL10/CXCR3 axis and pain (27). After partial infraorbital nerve ligation injury, the TG of mice showed significantly higher levels of CXCR3 mRNA on days 3, 10, and 21 (when the experiment terminated); CXCR3 protein was also significantly upregulated on day 10 after injury as seen by WB.…”

Section: Cxcl10/cxcr3mentioning

confidence: 64%

“…In vivo studies further support a direct role of the CXCL10/CXCR3 chemokine axis in pain ( 27 ). Intra-ganglionic injection of CXCL10 generated hypersensitivity, as measured by head withdrawal threshold.…”

Section: Direct Evidence Of Chemokines In Trigeminal Painmentioning

confidence: 90%

“…After partial infraorbital nerve ligation injury, the TG of mice showed significantly higher levels of CXCR3 mRNA on days 3, 10, and 21 (when the experiment terminated); CXCR3 protein was also significantly upregulated on day 10 after injury as seen by WB. Furthermore, mRNA for the ligand CXCL10 was also upregulated on day 3 and 10 after injury, and both ligand and receptor were detected on TG neurons labelled with TUBIII ( 27 ) ( Figure 1B ). The higher chemokine axis levels associated with the injury suggests a pronociceptive effect of the chemokine and its receptor.…”

Section: Direct Evidence Of Chemokines In Trigeminal Painmentioning

confidence: 99%

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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: Cxcl10/cxcr3mentioning

confidence: 64%

Section: Direct Evidence Of Chemokines In Trigeminal Painmentioning

confidence: 90%

Section: Direct Evidence Of Chemokines In Trigeminal Painmentioning

confidence: 99%

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Chemokines and Pain in the Trigeminal System

2021

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“…CXCL10 exerts its function by binding to its receptor CXCR3, which is a G protein-coupled receptor, which is expressed in a variety of cells such as lymphocytes and monocytes [23]. Recent studies showed that CXCR3 exists on mast cells in acute lung injury and chronic lung disease [24]. In addition, CXCL10 and CXCR3 continuously activate the oxidative burst and chemotaxis of mast cells in the form of an autocrine ring.…”

Section: Discussionmentioning

confidence: 99%

High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

Xie

Zheng

Mou

et al. 2022

BioMed Research International

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Background. The energy delivered by a ventilator to the respiratory system in one minute is defined as mechanical power (MP). However, the effect of ventilator-induced lung injury (VILI) in patients suffering from acute respiratory distress syndrome (ARDS) is still unknown. Our previous studies revealed that CXCL10 may be a potential biomarker of lung injury in ARDS. Therefore, the aim of this study was to compare the lung injury of rats and patients under different MP conditions to explore the involvement of CXCL10 and its receptor CXCR3 in VILI. Methods. Patients were divided into the high mechanical power group (HMPp group) and low mechanical power group (LMPp group), while rats were assigned to the high mechanical power group (HMPr group), medium mechanical power group (MMPr group), and low mechanical power group (LMPr group). CXCL10 and CXCR3 plasma content in ARDS patients and rats under ventilation at different MP was measured, as well as their protein and mRNA expression in rat lungs. Results. CXCL10 and CXCR3 content in the plasma of ARDS patients in the HMPp was significantly higher than that in the LMPp. The increase of MP during mechanical ventilation in the rats gradually increased lung damage, and CXCL10 and CXCR3 levels in rat plasma gradually increased with the increase of MP. CXCL10 and CXCR3 protein and mRNA expression in the HMPr group and MMPr group was significantly higher than that in the LMPr group ( P < 0.05 ). More mast cells were present in the trachea, bronchus, blood vessels, and lymphatic system in the rat lungs of the HMPr group, and the number of mast cells in the HMPr group ( 13.32 ± 3.27 ) was significantly higher than that in the LMPr group ( 3.25 ± 0.29 ) ( P < 0.05 ). Conclusion. The higher the MP, the more severe the lung injury, and the higher the CXCL10/CXCR3 expression. Therefore, CXCL10/CXCR3 might participate in VILI by mediating mast cell chemotaxis.

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“…Recent studies showed that CXCR3 exists on mast cells in acute lung injury and chronic lung disease [21]. In addition, CXCL10 and CXCR3 continuously activate the oxidative burst and chemotaxis of mast cells in the form of an autocrine ring.…”

Section: Cxcl10 and Cxcr3 Protein Expression In The Rat Lung Tissuementioning

confidence: 99%

High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

Xie

Zheng

Mou

et al. 2021

Preprint

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Background: The energy delivered by a ventilator to the respiratory system in one minute is defined as mechanical power (MP). However, the effect of the ventilator-induced lung injury (VILI) in patients suffering of acute respiratory distress syndrome (ARDS) is still unknown. Our previous studies revealed that CXCL10 may be a potential biomarker of lung injury in ARDS. Therefore, the aim of this study was to compare the lung injury of rats and patients under different MP conditions to explore the involvement of CXCL10 and its receptor CXCR3 in VILI. Methods: Patients were divided into high mechanical power group (HMP) and low mechanical power group (LMP), while rats were assigned to the high mechanical power group (HMP), medium mechanical power group (MMP) and low mechanical power group (LMP). CXCL10 and CXCR3 plasma content in ARDS patients and rats under ventilation at different MP was measured, as well as their protein and mRNA expression in rat lungs. Results: CXCL10 and CXCR3 content in the plasma of ARDS patients in the HMP was significantly higher than that in the LMP. The increase of MP during mechanical ventilation in the rats gradually increased lung damage, and CXCL10 and CXCR3 level in rat plasma gradually increased with the increase of MP. CXCL10 and CXCR3 protein and mRNA expression in the HMP group and MMP group was significantly higher than that in the LMP group (P<0.05). More mast cells were present in the trachea, bronchus, blood vessels, and lymphatic system in the rat lungs of the HMP group and the number of mast cells in the HMP group (13.32±3.27) was significantly higher than that in the LMP group (3.25±0.29) (P＜0.05). Conclusion: The higher the MP, the more severe the lung injury, the higher CXCL10/CXCR3 expression. Therefore, CXCL10/CXCR3 might participate in VILI by mediating mast cell chemotaxis.

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CXCL10 and CXCR3 in the Trigeminal Ganglion Contribute to Trigeminal Neuropathic Pain in Mice

Cited by 20 publications

References 47 publications

Chemokines and Pain in the Trigeminal System

Chemokines and Pain in the Trigeminal System

High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

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