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Soluble gp130 regulatess interleukin-6 in cerebrospinal fluid after subarachnoid haemorrhage
  1. Takahiro Nakura,
  2. Koji Osuka,
  3. Takashi Inukai,
  4. Teruhide Takagi,
  5. Masakazu Takayasu
  1. Department of Neurological Surgery, Aichi Medical University, Japan
  1. Correspondence to Dr Koji Osuka, Department of Neurological Surgery, Aichi Medical University,21 Karimata Yazako, Nagakute, Aichi-gun, 480-1195, Japan; kosuka{at}aichi-med-u.ac.jp

Abstract

Background Interleukin-6 (IL-6) is a proinflammatory cytokine reported to play an important role in induction of cerebral vasospasm after subarachnoid haemorrhage (SAH). Soluble gp130 (sgp130) and soluble IL-6 receptor (sIL-6R) are known to act as signal transducing receptors of IL-6, the former as an antagonist and the latter as an agonist. However, there have been no reports concerning regulation of the IL-6 signalling pathway in cerebrospinal fluid (CSF) after SAH.

Mehods Concentrations of IL-6, sgp130 and sIL-6R were measured serially until day 14 in CSF from nine patients with SAH. CSF samples obtained from patients suffering from unruptured aneurysm were used as controls. Colocalisation of IL-6 and sgp130 in CSF on day 1 was further examined by immunoprecipitaiton.

Results Concentrations of IL-6 in CSF increased immediately after the onset of SAH and remained chronically elevated over control values. Both sgp130 and sIL-6R also exhibited increased on day 1, followed by a decrease limited to the gp130 case after day 5. Sgp130 coimmunoprecipitated with IL-6 in CSF on day 1 after SAH.

Conclusions Our findings suggest that sgp130 regulates IL-6 signalling as an antagonist in CSF immediately after SAH. As the concentration of sgp130 decreases after day 5, IL-6 signals might then be more easily transmitted, presumably resulting in cerebral vasospasm.

  • Soluble gp130
  • soluble interleukin-6 receptor
  • subarachnoid haemorrhage
  • CSF

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Footnotes

  • Competing interests None.

  • Ethics approval Ethics approval was provided by the Aichi Medical University.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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