The present study presents galectin-3 as a new molecule involved in the spinal processes of acute herpetic pain in mice.
To identify endogenous factors involved in herpetic pain, we performed genome-wide microarray analysis of the spinal cord of mice that suffered from herpetic allodynia induced by inoculation with herpes simplex virus type 1, which revealed marked induction of galectin-3, a β-galactoside-binding lectin. Therefore, we investigated the role of galectin-3 in herpetic allodynia. The expression levels of galectin-3 mRNA and protein were increased with a temporal pattern similar to that of herpetic allodynia. Galectin-3-expressing cells were mainly localized in the superficial dorsal horn, round in shape, and positive for the macrophage/microglia markers Iba-1 and F4/80. In the deep dorsal horn, there were Iba-1-positive cells with ramified and stout processes, which were negative for galectin-3. In the superficial dorsal horn, there were many CD3-positive T cells, but most of the galectin-3-expressing cells were negative for CD3. Galectin-3-expressing cells were negative for the neuronal marker NeuN and the astrocyte marker glial fibrillary acidic protein antibody. Deficiency in galectin-3 markedly reduced herpetic allodynia, without showing an effect on herpes zoster-like skin lesions. Intrathecal injection of galectin-3 produced mechanical allodynia in naive mice, and intrathecal injections of anti-galectin-3 antibodies significantly reduced herpetic allodynia. The present results suggest that galectin-3 in infiltrating macrophages and/or resident microglia in the spinal dorsal horn contributes to herpetic allodynia. Galectin-3 may be a new therapeutic target for the treatment of herpes zoster-associated pain.
aDivision of Molecular Genetics Research, Life Science Research Center, University of Toyama, Toyama, Japan
bDepartment of Applied Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan
cDepartment of Pharmacology, School of Pharmaceutical Sciences, Ohu University, Koriyama, Fukushima, Japan
dDepartment of Virology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan
eDepartment of Dermatology, University of California, Davis, School of Medicine, Sacramento, CA, USA
fDepartment of Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan
*Corresponding author. Address: Sugitani 2630, Toyama 930-0194, Japan. Tel.: +81 76 434 7510; fax: +81 76 434 5045.
Submitted May 17, 2011; revised and accepted November 18, 2011.