한빛사논문
Jaesung Lee a,c, Giljae Lee b, Gwangpyo Ko b, Sung Joong Lee a,c
aDepartment of Neuroscience and Physiology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul, Republic of Korea
bDepartment of Environmental Health Sciences, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea
cInterdisciplinary Program in Neuroscience, College of Natural Science, Seoul National University, Seoul, Republic of Korea
Corresponding author: Sung Joong Lee
Abstract
The impact of the gut microbiota on glial cell growth and maturation via the gut-brain axis is highlighted herein. Considering that glial activation is crucial for onset and maintenance of neuropathic pain, we assessed the putative involvement of gut microbiota in the pathogenesis of neuropathic pain. Depletion of mouse gut microbiota with chronic antibiotics cocktail treatment prevented nerve injury-induced mechanical allodynia and thermal hyperalgesia both in male and female mice. Furthermore, post-injury treatment with antibiotics cocktail relieved ongoing pain in neuropathic pain-established mice. Upon recolonization of the gut microbiota after cessation of antibiotics, nerve injury-induced mechanical allodynia relapsed. Depletion of gut microbiota accompanied a decrease in nerve injury-induced TNF-α expression in the spinal cord. Notably, nerve injury changed the diversity and composition of the gut microbiome, which was measured by 16 s rRNA sequencing. We then tested if probiotic administration ameliorating dysbiosis affected the development of neuropathic pain after nerve injury. Probiotic treatment for three weeks prior to nerve injury inhibited nerve injury-induced TNF-α expression in the spinal cord and pain sensitization. Our data reveal an unexpected link between the gut microbiota and development and maintenance of nerve injury-induced neuropathic pain, and we propose a novel strategy to relieve neuropathic pain through the gut-brain axis.
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