부산대학교 도서관

Background: The involvement of inflammation in the pathophysiology of cluster headache (CH) has been suggested, with a role implied for interleukin (IL)‐1β. We aimed to measure peripheral blood expression levels of IL‐1β–inducing systems, the inflammasome complex, and nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling, and investigate their values as putative biomarkers in CH. Methods: In this cross‐sectional study conducted in the Headache Unit of Istanbul University, Turkey, blood mononuclear cells (PBMCs) and sera were collected from 30 patients with episodic migraine, 4 with chronic CH, and 47 healthy individuals. Levels of inflammasome complex components (NLRP1, NLRP3, caspase 1, and ASC), end products of inflammasome complex activity (IL‐1β, IL‐18, and nitric oxide synthase isoforms), neuron‐specific enolase, other inflammatory factors (NF‐κB, HMGB1, and s100b), and anti‐inflammatory IL‐4 were measured by real‐time quantitative polymerase chain reaction and/or enzyme‐linked immunosorbent assay. Results: NLRP3 expression levels were significantly reduced in PBMC samples of patients with CH, obtained during CH attacks (n = 24) or headache‐free (out of cycle) episodes (n = 10). CH‐attack patients showed greater expression levels of IL‐1β (2−ΔΔCT median [25th–75th percentile], 0.96 [0.66–1.29 vs. 0.52 [0.43–0.73]) and NF‐κB (1.06 [0.66–3.00] vs. 0.62 [0.43–1.19]) in PBMCs but not in sera compared with headache‐free CH patients. However, these differences did not attain statistical significance (p = 0.058 and p = 0.072, respectively). Moreover, NLRP1 (52.52 [35.48–67.91] vs. 78.66 [54.92–213.25]; p = 0.017), HMGB1 (11.51 [5.20–15.50] vs. 13.33 [8.08–18.13]; p = 0.038), S100b (569.90 [524.10–783.80] vs. 763.40 [590.15–2713.00]; p = 0.013), NSE (11.15 [6.26–14.91] vs. 13.93 [10.82–19.04]; p = 0.021), nNOS (4.24 [3.34–12.85] vs. 12.82 [4.52–15.44]; p = 0.028), and eNOS (64.83 [54.59–91.14] vs. 89.42 [61.19–228.40]; p = 0.034) levels were lower in patients with three or more autonomic manifestations (n = 9). No correlation was found between inflammation factors and clinical parameters of CH. Conclusion: Our results support the involvement of the IL‐1β system in attacks of CH. However, the components of the inflammasome complex are suppressed in the peripheral blood and do not appear to play a role in the pathophysiology of CH. These findings argue against a potential biomarker value of the inflammasome complex in CH. [ABSTRACT FROM AUTHOR]