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Interleukin‐2 gene expression in different phases of episodic cluster headache – a pilot study
Author(s) -
Steinberg A.,
Sjöstrand C.,
Sominanda A.,
FogdellHahn A.,
Nilsson Remahl A. I. M.
Publication year - 2011
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2010.01434.x
Subject(s) - pathophysiology , medicine , venous blood , cluster headache , cytokine , immune system , gastroenterology , interleukin , immunology , endocrinology , migraine
Steinberg A, Sjöstrand C, Sominanda A, Fogdell‐Hahn A, Nilsson Remahl AIM. Interleukin‐2 gene expression in different phases of episodic cluster headache – a pilot study.
Acta Neurol Scand: 2011: 124: 130–134.
© 2010 John Wiley & Sons A/S. 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.