Exploring the role of inflammatory biomarkers in trigeminal neuralgia
Background: Trigeminal neuralgia (TN) is a severe facial pain disorder with complex etiology. Inflammation has been suggested as a contributing factor to TN pathogenesis. This study investigates the causal relationship between inflammatory biomarkers, including 41 circulating inflammatory cytokines,...
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Elsevier
2025-02-01
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| Series: | Brain, Behavior, & Immunity - Health |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2666354624002084 |
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| author | Shenglong Lai Haiyang Li Yazhou Xing Du Wu Lin Wang Qinghua Liang |
| author_facet | Shenglong Lai Haiyang Li Yazhou Xing Du Wu Lin Wang Qinghua Liang |
| author_sort | Shenglong Lai |
| collection | DOAJ |
| description | Background: Trigeminal neuralgia (TN) is a severe facial pain disorder with complex etiology. Inflammation has been suggested as a contributing factor to TN pathogenesis. This study investigates the causal relationship between inflammatory biomarkers, including 41 circulating inflammatory cytokines, C-reactive protein (CRP), and procalcitonin (PCT), and TN using Mendelian randomization (MR) analysis. Methods: A two-sample MR approach was employed using genome-wide association study (GWAS) data from 8293 Finnish individuals for inflammatory cytokines and data from the FinnGen database for TN. Instrumental variables (IVs) were selected based on genome-wide significance and clumping thresholds to avoid linkage disequilibrium. Inverse variance weighting (IVW) was used as the primary method, complemented by MR Egger regression, weighted median, simple mode, and weighted mode methods. Additionally, Bayesian Weighted MR (BWMR) and Multivariable MR (MVMR) were utilized to validate the findings and explore potential confounders. Results: The present MR analysis identified significant causal associations for three inflammatory cytokines with TN. Stem cell growth factor beta (SCGF-β) (OR = 1.362, 95% CI = 1.049–1.770, p = 0.021) and Interleukin-4 (IL-4) (OR = 1.533, 95% CI = 1.014–2.316, p = 0.043) were positively associated with TN, while Interleukin-16 (IL-16) (OR = 0.720, 95% CI = 0.563–0.921, p = 0.009) had a protective effect. CRP levels were also linked to TN risk (OR = 0.751, 95% CI = 0.593–0.951, p = 0.017). No significant causal effect of PCT on TN was observed. Sensitivity analyses confirmed the robustness of these findings, showing no evidence of horizontal pleiotropy or heterogeneity. Conclusion: This study highlights specific inflammatory biomarkers that may play pivotal roles in TN pathogenesis. SCGF-β and IL-4 are potential therapeutic targets due to their facilitative effects on TN, while IL-16 could offer protective benefits. CRP's association with TN further supports the involvement of systemic inflammation in this condition. These findings provide novel insights into TN's inflammatory mechanisms, suggesting new avenues for targeted interventions. |
| format | Article |
| id | doaj-art-f102736bb53a4e0fb949ece9a1009f5c |
| institution | Kabale University |
| issn | 2666-3546 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Brain, Behavior, & Immunity - Health |
| spelling | doaj-art-f102736bb53a4e0fb949ece9a1009f5c2025-01-26T05:05:02ZengElsevierBrain, Behavior, & Immunity - Health2666-35462025-02-0143100930Exploring the role of inflammatory biomarkers in trigeminal neuralgiaShenglong Lai0Haiyang Li1Yazhou Xing2Du Wu3Lin Wang4Qinghua Liang5Department of Neurosurgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, 450003, ChinaDepartment of Neurosurgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, 450003, ChinaDepartment of Neurosurgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, 450003, ChinaDepartment of Neurosurgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, 450003, ChinaDepartment of Neurosurgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, 450003, ChinaCorresponding author.; Department of Neurosurgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, 450003, ChinaBackground: Trigeminal neuralgia (TN) is a severe facial pain disorder with complex etiology. Inflammation has been suggested as a contributing factor to TN pathogenesis. This study investigates the causal relationship between inflammatory biomarkers, including 41 circulating inflammatory cytokines, C-reactive protein (CRP), and procalcitonin (PCT), and TN using Mendelian randomization (MR) analysis. Methods: A two-sample MR approach was employed using genome-wide association study (GWAS) data from 8293 Finnish individuals for inflammatory cytokines and data from the FinnGen database for TN. Instrumental variables (IVs) were selected based on genome-wide significance and clumping thresholds to avoid linkage disequilibrium. Inverse variance weighting (IVW) was used as the primary method, complemented by MR Egger regression, weighted median, simple mode, and weighted mode methods. Additionally, Bayesian Weighted MR (BWMR) and Multivariable MR (MVMR) were utilized to validate the findings and explore potential confounders. Results: The present MR analysis identified significant causal associations for three inflammatory cytokines with TN. Stem cell growth factor beta (SCGF-β) (OR = 1.362, 95% CI = 1.049–1.770, p = 0.021) and Interleukin-4 (IL-4) (OR = 1.533, 95% CI = 1.014–2.316, p = 0.043) were positively associated with TN, while Interleukin-16 (IL-16) (OR = 0.720, 95% CI = 0.563–0.921, p = 0.009) had a protective effect. CRP levels were also linked to TN risk (OR = 0.751, 95% CI = 0.593–0.951, p = 0.017). No significant causal effect of PCT on TN was observed. Sensitivity analyses confirmed the robustness of these findings, showing no evidence of horizontal pleiotropy or heterogeneity. Conclusion: This study highlights specific inflammatory biomarkers that may play pivotal roles in TN pathogenesis. SCGF-β and IL-4 are potential therapeutic targets due to their facilitative effects on TN, while IL-16 could offer protective benefits. CRP's association with TN further supports the involvement of systemic inflammation in this condition. These findings provide novel insights into TN's inflammatory mechanisms, suggesting new avenues for targeted interventions.http://www.sciencedirect.com/science/article/pii/S2666354624002084Trigeminal neuralgiaInflammatory biomarkersMendelian randomizationCytokinesC-Reactive protein |
| spellingShingle | Shenglong Lai Haiyang Li Yazhou Xing Du Wu Lin Wang Qinghua Liang Exploring the role of inflammatory biomarkers in trigeminal neuralgia Brain, Behavior, & Immunity - Health Trigeminal neuralgia Inflammatory biomarkers Mendelian randomization Cytokines C-Reactive protein |
| title | Exploring the role of inflammatory biomarkers in trigeminal neuralgia |
| title_full | Exploring the role of inflammatory biomarkers in trigeminal neuralgia |
| title_fullStr | Exploring the role of inflammatory biomarkers in trigeminal neuralgia |
| title_full_unstemmed | Exploring the role of inflammatory biomarkers in trigeminal neuralgia |
| title_short | Exploring the role of inflammatory biomarkers in trigeminal neuralgia |
| title_sort | exploring the role of inflammatory biomarkers in trigeminal neuralgia |
| topic | Trigeminal neuralgia Inflammatory biomarkers Mendelian randomization Cytokines C-Reactive protein |
| url | http://www.sciencedirect.com/science/article/pii/S2666354624002084 |
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