Expression of the Mu Opioid Receptor in the Human Immunodeficiency Virus Type 1 Transgenic Rat Model

Chang, Sulie L.; Beltrán, José Eduardo Padilla; Swarup, Shilpa

doi:10.1128/jvi.00155-07

Cited by 29 publications

(29 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inflammatory cytokines such as IL-6 (Borner et al 2004a, b) and TNF-α (Borner et al 2007) induce MOR expression in lymphocytes, and several transcription factors participate in regulation of MOR expression including Stat6 and Gata3 (Kraus et al 2001(Kraus et al , 2003Borner et al 2004aBorner et al , b, 2006. Other factors, such as human immunodeficiency virus gp120, can transactivate MOR gene expression (Chang et al 2007). A recent study demonstrated that MOR mRNA was induced after CD3/28-mediated activation of primary human T lymphocytes, and transcriptional induction was proceeded by activator protein-1 (AP-1), nuclear factor-κB (NF-κB), and nuclear factor of activated T cells (Borner et al 2008).…”

Section: Discussionmentioning

confidence: 98%

Inducible Expression of Functional Mu Opioid Receptors in Murine Dendritic Cells

Chu

Shan³

et al. 2009

J Neuroimmune Pharmacol

View full text Add to dashboard Cite

Opioids are known to exert direct effects on the immune system, and the expression of functional opioid receptors has been reported on several immune cell types. Dendritic cells (DCs) are important inducers and regulators of immune responses. In this study, we investigated whether murine dendritic cells express functional mu opioid receptors (MOR). RT-PCR analysis and double immunofluorescence staining revealed the expression of MOR in activated murine dendritic cells. We also studied the dynamic expression of MOR messenger RNA in murine dendritic cells in response to different Toll-like receptor ligands. Functionally, treatment of DCs with endomorphin 1 (EM1), a specific agonist of MOR, can inhibit the forskolin-induced formation of cyclic adenosine monophosphate level in activated DCs. Moreover, EM1 treatment resulted in less activation of p38 MAPK and more activation of ERK signaling in lipopolysaccharide-stimulated DCs. Consistently, treatment of DCs with EM1 altered cytokine production by increasing IL-10 and decreasing IL-12 and IL-23. Our results suggest that MOR is inducibly expressed on activated DCs and functionally mediates EM1-induced effects on DCs. Thus, dendritic cells might be involved in crosstalk between the neuroendocrine and the immune system.

show abstract

Section: Discussionmentioning

confidence: 98%

Inducible Expression of Functional Mu Opioid Receptors in Murine Dendritic Cells

Chu

Shan³

et al. 2009

J Neuroimmune Pharmacol

View full text Add to dashboard Cite

show abstract

“…The purpose of the early inflammatory response by macrophages is to eliminate invading microbes by recruiting leukocytes to the site of infection and to initiate a balance of pro- and anti-inflammatory cytokines. In the HIV-1Tg rat, the TLR-stimulated immune response to the bacterial endotoxin, lipopolysaccharide (LPS), is altered (Chang, Beltran et al 2007; Chang, Ocasio et al 2007). LPS fails to initiate the adhesion of leukocytes to the endothelial cell walls, the first step by which leukocytes migrate through the endothelium of post-capillary venules to the site of infection (Chang, Ocasio et al 2007).…”

Section: The Hiv-1tg Rat As a Model Of Neurohivmentioning

confidence: 99%

“…LPS fails to initiate the adhesion of leukocytes to the endothelial cell walls, the first step by which leukocytes migrate through the endothelium of post-capillary venules to the site of infection (Chang, Ocasio et al 2007). Blood plasma levels of TNF-α and IL1-β are greater in the HIV-1Tg rat compared to control animals (Chang, Beltran et al 2007), and the balance between pro- and anti-inflammatory cytokines and chemokines is substantially altered in response to an endotoxin challenge in the HIV-1Tg rat (Homji 2012). Monocytes and macrophages are also the principle cells responsible for endotoxin tolerance (Cavaillon 2006).…”

Section: The Hiv-1tg Rat As a Model Of Neurohivmentioning

confidence: 99%

“…LPS was used to induce IL-1β, IL-10, and TNF-α, all of which have been shown to modulate MOR expression (Borner, Kraus et al 2004; Kraus 2009). TNF-α and IL-1β levels were increased 7- and 38-fold, respectively, by LPS in HIV-1Tg rats compared to control rats (Chang, Beltran et al 2007). MOR expression was also examined in response to LPS treatment.…”

Section: Behavioral Alterations In the Hiv-1tg Ratmentioning

confidence: 99%

See 1 more Smart Citation

The HIV-1 transgenic rat model of neuroHIV

Vigorito

Connaghan

Chang

2015

Brain, Behavior, and Immunity

Self Cite

View full text Add to dashboard Cite

Despite the ability of current combination anti-retroviral therapy (cART) to limit the progression of HIV-1 to AIDS, HIV-positive individuals continue to experience neuroHIV in the form of HIV-associated neurological disorders (HAND), which can range from subtle to substantial neurocognitive impairment. NeuroHIV may also influence substance use, abuse, and dependence in HIV-positive individuals. Because of the nature of the virus, variables such as mental health co-morbidities make it difficult to study the interaction between HIV and substance abuse in human populations. Several rodent models have been developed in an attempt to study the transmission and pathogenesis of the HIV-1 virus. The HIV-1 transgenic (HIV-1Tg) rat is a reliable model of neuroHIV because it mimics the condition of HIV-infected patients on cART. Research using this model supports the hypothesis that the presence of HIV-1 viral proteins in the central nervous system increases the sensitivity and susceptibility of HIV-positive individuals to substance abuse.

show abstract

“…Tail-flick latencies are significantly longer in the HIV-1Tg rat following treatment with morphine, and the ED50 of morphine is lower in HIV-1Tg rats than in control rats , suggesting that the HIV-1Tg rat is more prone to the antinociceptive and rewarding properties of opioids. One of the possible molecular mechanisms underlying the increase in tail-flick latency is the increased expression of the MOR in the HIV-1Tg rat (Chang, Beltran, & Swarup, 2007;. Chang and Connaghan (2012) provided further behavioral evidence of a link between morphine and neuroHIV.…”

Section: Morphine and Neurohivmentioning

confidence: 97%