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Interleukin-2 gene expression in different phases of episodic cluster headache--a pilot study
A Steinberg1, C Sjöstrand, A Sominanda
1Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden. anna.steinberg@karolinska.s
Insights
Interleukin-2 (IL-2) gene expression is significantly elevated between cluster headache attacks, suggesting a role for the immune system in this condition. Further research into cytokines and larger patient groups is recommended.
Area of Science:
- Neurology
- Immunology
- Molecular Biology
Background:
- The underlying causes of cluster headache (CH) remain largely unclear.
- Immune system involvement is a suspected factor in CH pathophysiology.
Purpose of the Study:
- To evaluate interleukin-2 (IL-2) as a potential biomarker for immune system activity in CH.
- To investigate the role of IL-2 in the pathophysiology of cluster headaches.
Main Methods:
- Quantitative real-time polymerase chain reaction was used to analyze IL-2 gene expression.
- Blood samples were collected from 8 episodic CH patients during active periods, attacks, and remission, and from 16 healthy controls.
Main Results:
- Significantly higher IL-2 gene expression was observed in CH patients during active periods between attacks compared to during attacks, remission, and controls.
- IL-2 levels were markedly elevated between attacks in the active phase of cluster headache.
Conclusions:
- Elevated IL-2 during active cluster headache periods supports the involvement of this cytokine and the immune system in CH.
- Further studies with larger cohorts and a wider range of cytokines are needed to confirm these findings.
Background:
The pathophysiology of cluster headache (CH) is still largely unknown. Immunological mechanisms have been suggested to be of importance.
Aim:
This study aimed to investigate cytokine interleukin-2 (IL-2) as a possible marker of immune system involvement in the pathophysiology of CH.
Methods:
Eight episodic patients with CH and 16 healthy headache-free control subjects matched for age and gender were studied. Venous blood samples were drawn from the patients with CH on three occasions; during active period between headache attacks, during an attack and in remission. Venous blood samples were drawn once from each control subject. We analysed IL-2 gene expression, using quantitative real-time polymerase chain reaction.
Results:
Patients with CH had significantly increased relative IL-2 gene expression levels between headache attacks during active CH period (median 9.9 IL-2 cDNA/glyceraldehyde-3-phosphate dehydrogenase cDNA; IQR 6.2-10.3) compared to during attacks (median 2.8; IQR 0.7-3.2, P = 0.012), remission (median 1.6; IQR 0.9-1.8, P = 0.017) and controls (median 0.9; IQR 0.6-1.9, P = 0.0001).
Conclusion:
The increment of IL-2 found during the active CH period may support a role for this cytokine and subsequently for the immune system in the pathophysiology of CH. An expansion of this study to a broader group of cytokines and a larger patient cohort is warranted.
