PMC:7463108 / 93932-95637 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7463108","sourcedb":"PMC","sourceid":"7463108","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7463108","text":"Postmortem clinical studies indicate the endogenous opioid system is disrupted in neuroHIV (Gelman et al. 2012; Yuferov et al. 2014). Specifically, OPRK1 mRNA is significantly upregulated in PWH (Yuferov et al. 2014) and in transgenic neuroHIV rodent models (Chang et al. 2007; Fitting et al. 2010b) potentially as a compensatory neuroprotective function in response to inflammatory processes in the presence of HIV infection (Yuferov et al. 2014). The upregulation of mRNA coding OPRK1 is triggered by factors released by activated macrophages and glia and is supported by mechanistic studies in dorsal root ganglia (Puehler et al. 2006; Gabrilovac et al. 2012). Since leukocytes, including macrophages, can express β-endorphin and enkephalins, it is important to consider the potential influence of leukocyte-derived endogenous opioid peptides in neuroinflammation (Rittner et al. 2001). Granulocytes express about 10-fold higher levels of β-endorphin, a preferential MOR and lower affinity KOR endogenous ligand, than lymphocytes (Pallinger and Csaba 2008). Increases in β-endorphin expression by peripheral blood mononuclear cells (PBMCs) (Gironi et al. 2000; Gironi et al. 2003), coincide with inflammation and relapse in multiple sclerosis. Moreover, increases in inflammatory cytokines, such as interleukin-1β (IL-1β), have been demonstrated to differentially increase the expression of proenkephalin transcripts in primary astrocytes cultured from different brain regions (Ruzicka and Akil 1997) and increase IL-10-stimulated β-endorphin expression in cultured primary microglia (Wu et al. 2017). 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