Chronic-pain-associated astrocytic reaction in the spinal cord dorsal horn of human immunodeficiency virus-infected patients

• Published in: The Journal of neuroscience Vol. 32; no. 32; pp. 10833 - 10840
• Main Authors: Shi, Yuqiang, Gelman, Benjamin B, Lisinicchia, Joshua G, Tang, Shao-Jun
• Format: Journal Article
• Language: English
• Published: United States Society for Neuroscience 08.08.2012
• Subjects: Adult; Analysis of Variance; Astrocytes - metabolism; Astrocytes - pathology; CD11b Antigen - metabolism; Cell Count; Chronic Pain - etiology; Chronic Pain - pathology; Chronic Pain - virology; Glial Fibrillary Acidic Protein - metabolism; HIV Infections - complications; HIV Infections - pathology; Human immunodeficiency virus; Humans; Interleukin-1beta - metabolism; Male; MAP Kinase Signaling System - physiology; Middle Aged; Nerve Growth Factors - metabolism; Nerve Tissue Proteins - metabolism; Postmortem Changes; S100 Calcium Binding Protein beta Subunit; S100 Proteins - metabolism; Spinal Cord - pathology; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0270-6474; 1529-2401; 1529-2401
• DOI: 10.1523/jneurosci.5628-11.2012

Studies with animal models have suggested that reaction of glia, including microglia and astrocytes, critically contributes to the development and maintenance of chronic pain. However, the involvement of glial reaction in human chronic pain is unclear. We performed analyses to compare the glial reaction profiles in the spinal dorsal horn (SDH) from three cohorts of sex- and age-matched human postmortem tissues: (1) HIV-negative patients, (2) HIV-positive patients without chronic pain, and (3) HIV patients with chronic pain. Our results indicate that the expression levels of CD11b and Iba1, commonly used for labeling microglial cells, did not differ in the three patient groups. However, GFAP and S100β, often used for labeling astrocytes, were specifically upregulated in the SDH of the "pain-positive" HIV patients but not in the "pain-negative" HIV patients. In addition, proinflammatory cytokines, TNFα and IL-1β, were specifically increased in the SDH of pain-positive HIV patients. Furthermore, proteins in the MAPK signaling pathway, including pERK, pCREB and c-Fos, were also upregulated in the SDH of pain-positive HIV patients. Our findings suggest that reaction of astrocytes in the SDH may play a role during the maintenance phase of HIV-associated chronic pain.