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Editors Selection IGR 7-1

Basic Research: IL-6, a protective cytokine

Comment by Rosario Hernandez on:

21756 Contribution of TRPV1 to microglia-derived IL-6 and N&Fkappa;B translocation with elevated hydrostatic pressure, Sappington RM; Calkins DJ, Investigative Ophthalmology and Visual Science, 2008; 49: 3004-3017

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Sappington and Calkins (980) report on the role of transient receptor potential vanilloid subtype 1 (TRPV1) and Ca²⁺ in the expression of IL-6 and nuclear factor kappa B (NFkB) translocation with elevated hydrostatic pressure in retinal microglia. TRPV1, known as 'capsaicin receptor', is a well studied nociceptor involved in pain and body temperature regulation. Katsura et al. (2006) reported that TRPV1 receptors in spinal cord microglia contribute to the development of mechanical hypersensitivity through the ERK pathway. Kim et al. (2006) reported that TRPV1, and activation of its receptor may contribute to microglial damage via Ca²⁺ signaling and mitochondrial disruption. The present study points to a novel function of the receptor in retinal microglia activation and release of IL-6 in response to elevated pressure in vivo and in vitro.

Activation of Ca²⁺ channels or transporters in response to hydrostatic pressure in retinal microglia leads to release of IL-6, a protective cytokine for retinal ganglion cells

To establish relevance to glaucoma in vivo, the authors first demonstrated that in the hereditary mouse glaucoma model, DBA-2 mouse, IL-6 was expressed in microglial cells at the onset of elevated IOP in the retina. TRPV1 was demonstrated in isolated rat retinal microglia and in whole mounts of rat retinas. The authors confirmed previous published data that activation of retinal microglia involves NFkB activation and increased release of IL-6 in response to elevated hydrostatic pressure. The data strongly suggest that Ca²⁺ signaling is involved in the IL-6/NFkB response to hydrostatic pressure in microglia. Pharmacological antagonists of TRVP1 blocked partially the effects of hydrostatic pressure on IL-6 release and NFkB activation. This paper provides a mechanism by which Ca²⁺ channels or transporters activation in response to hydrostatic pressure in retinal microglia lead to release of IL-6, a protective cytokine for retinal ganglion cells. The data presented are novel, because they underscore microglia as a potential target for neuroprotection in glaucoma.

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