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Interleukin-18-mediated microglia/astrocyte interaction in the spinal cord enhances neuropathic pain processing after nerve injury.

Authors: Miyoshi, K  Obata, K  Kondo, T  Okamura, H  Noguchi, K 
Citation: Miyoshi K, etal., J Neurosci. 2008 Nov 26;28(48):12775-87. doi: 10.1523/JNEUROSCI.3512-08.2008.
Pubmed: (View Article at PubMed) PMID:19036970
DOI: Full-text: DOI:10.1523/JNEUROSCI.3512-08.2008

Interleukin (IL)-18 is an important regulator of innate and acquired immune responses. Here we show that both the IL-18 and IL-18 receptor (IL-18R), which are induced in spinal dorsal horn, are crucial for tactile allodynia after nerve injury. Nerve injury induced a striking increase in IL-18 and IL-18R expression in the dorsal horn, and IL-18 and IL-18R were upregulated in hyperactive microglia and astrocytes, respectively. The functional inhibition of IL-18 signaling pathways suppressed injury-induced tactile allodynia and decreased the phosphorylation of nuclear factor kappaB in spinal astrocytes and the induction of astroglial markers. Conversely, intrathecal injection of IL-18 induced behavioral, morphological, and biochemical changes similar to those observed after nerve injury. Our results indicate that IL-18-mediated microglia/astrocyte interactions in the spinal cord have a substantial role in the generation of tactile allodynia. Thus, blocking IL-18 signaling in glial cells might provide a fruitful strategy for treating neuropathic pain.


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RGD Object Information
RGD ID: 8655929
Created: 2014-05-23
Species: All species
Last Modified: 2014-05-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.