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The Journal of Neuroscience, May 17, 2006, 26(20):5565-5573; doi:10.1523/JNEUROSCI.0815-06.2006

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Development/Plasticity/Repair
The Cytokine Interleukin-6 Is Sufficient But Not Necessary to Mimic the Peripheral Conditioning Lesion Effect on Axonal Growth

Zixuan Cao,¹ Ying Gao,¹ J. Barney Bryson,¹ Jianwei Hou,¹ Nagarathnamma Chaudhry,¹ Mustafa Siddiq,¹ Jennifer Martinez,¹ Tim Spencer,¹ Jason Carmel,² Ronald B. Hart,² and Marie T. Filbin¹

¹Department of Biological Sciences, Hunter College, The City University of New York, New York, New York 10021, and ²W. M. Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854

Correspondence should be addressed to Dr. Marie T. Filbin, Department of Biological Sciences, Hunter College, The City University of New York, 695 Park Avenue, New York, NY 10021. Email: Filbin{at}genectr.hunter.cuny.edu

Lesioning the peripheral branch of a dorsal root ganglion (DRG) neuron before injury of the central branch of the same neuron enables spontaneous regeneration of these spinal axons. This effect is cAMP and transcription dependent. Here, we show that the cytokine interleukin-6 (IL-6) is upregulated in DRG neurons after either a conditioning lesion or treatment with dibutyryl-cAMP. In culture, IL-6 allows neurons to grow in the presence of inhibitors of regeneration present in myelin. Importantly, intrathecal delivery of IL-6 to DRG neurons blocks inhibition by myelin both in vitro and in vivo, effectively mimicking the conditioning lesion. Blocking IL-6 signaling has no effect on the ability of cAMP to overcome myelin inhibitors. Consistent with this, IL-6-deficient mice respond to a conditioning lesion as effectively as wild-type mice. We conclude that IL-6 can mimic both the cAMP effect and the conditioning lesion effect but is not an essential component of either response.

Key words: IL-6; conditioning lesion; regeneration; cAMP; microarray; cytokine

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Received Feb. 22, 2006; revised April 5, 2006; accepted April 11, 2006.

Correspondence should be addressed to Dr. Marie T. Filbin, Department of Biological Sciences, Hunter College, The City University of New York, 695 Park Avenue, New York, NY 10021. Email: Filbin{at}genectr.hunter.cuny.edu

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