PMC:7463108 / 92836-96886 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":"Does HIV Alter the Endogenous Opioid System?\nLittle is known about the effects of HIV on the endogenous opioid system and the extent to which HIV might disrupt the expression and function of opioid peptides and receptors, and vice versa. Because opiate drugs act exclusively by mimicking endogenous peptides and engaging opioid receptors, it is likely that endogenous opioids also interact with HIV to some extent to affect the pathogenesis of neuroHIV.\nThe endogenous opioid system comprises three originally described opioid receptors, MOR, KOR, and DOR and endogenous opioid peptide-expressing genes proopiomelanocortin (POMC), prodynorphin (PDYN), and proenkephalin (PENK) (Brownstein 1993; Trescot et al. 2008; Bodnar 2010; Pasternak and Pan 2013), as well as a fourth receptor (OPRN1) and peptide (nociceptin/orphanin FQ) family member. The endogenous opioid system has a fundamental role in pain regulation and has been implicated in the pathophysiology of various neurologic diseases (Nandhu et al. 2010; Sauriyal et al. 2011; Benarroch 2012) and in pain management (Bruehl et al. 2013).\nPostmortem 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). Interestingly, OPRM1 mRNA levels do not differ between HIV+ and HIV− subjects (Yuferov et al. 2014).\nPENK was downregulated in brain samples from 446 PWH compared to 67 HIV negative patients (Gelman et al. 2012). The subjects with HIV also expressed higher levels of interferon regulatory factor 1 (IRF1) transcripts. The idea that higher opioid peptide expression levels are neuroprotective has been supported in human studies and experimental animal models (Solbrig and Koob 2004; Sarkisyan et al. 2015; Nam et al. 2019) suggesting the reductions in PENK expression are deleterious.\nThe effects of HIV Tat on expression levels of opioid peptide and receptor levels depend on the individual CNS region involved as well as levels of tat transgene expression (Fitting et al. 2010b). For example, while PDYN mRNA levels were significantly reduced in the hippocampus and striatum of Tat-expressing mice, POMC was only significantly reduced by Tat induction in the striatum and PENK mRNA levels in the hippocampus were affected by chronic (but not acute) Tat exposure (Fitting et al. 2010b). Thus, HIV may alter the endogenous opioid system by modifying the expression of opioid peptides and their receptors in a brain- and cell-type specific manner. The consequences of HIV-1-dependent alterations in the endogenous opioid system to HAND are 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