Mu Opioid Receptor Gene Expression in Immune Cells

Chuang, Teddy K.; Killam, Keith F.; Chuang, Linda F.; Kung, Hsiang Fu; Sheng, Wen S.; Chao, Chun C.; Yu, Lei; Chuang, Ronald Y.

doi:10.1006/bbrc.1995.2709

Cited by 181 publications

(99 citation statements)

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“…Further incubation of SRV-infected cells up to 12 days in the presence of morphine had little effect on, or slightly decreased, viral infectivity, as again shown by RT assays (Table III). DISCUSSION Immune cells have been shown to express brain-like opioid receptors (22)(23)(24). Similar to chemokine receptors, opioid receptors are also G protein coupled, seven-transmembrane domain receptors (25).…”

Section: Infection Of Cem X174 Cells With Sivmac239 or Srv-methodsmentioning

confidence: 99%

Morphine Induces Gene Expression of CCR5 in Human CEM x174 Lymphocytes

Miyagi¹,

Chuang²,

Doi³

et al. 2000

Journal of Biological Chemistry

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All HIV-1 strains studied to date use CCR5, CXCR4, or both receptors to enter cells. Simian immunodeficiency virus (SIV) infection of non-human primates has served as a useful model for understanding AIDS pathogenesis in humans. Research on several genetically divergent SIV isolates has revealed that SIV uses CCR5, and not CXCR4, for entry. CEM x174, a human lymphoid cell line, has been routinely used to cultivate and maintain various SIV strains. However, questions have arisen about how CEM x174, which reportedly was unable to express detectable amounts of CCR5 transcripts, efficiently supports the growth of SIV. In searching for an answer, we resorted to a sensitive competitive reverse transcriptase-polymerase chain reaction procedure in an attempt to detect as well as quantify the amount of CCR5 expression. Here we present our findings, which indicate that CEM x174 indeed expresses CCR5 and that the amount of CCR5 is increased in cells pretreated with morphine. These results correlate well with our previous observations that morphine treatment causes CEM x174 cells to be more susceptible to SIV infection. Similar morphine effect was not observed on CEM x174 cells infected with simian retroviruses, which do not depend on CCR5 for entry. These findings suggest a plausible mechanism whereby opiate drug users render themselves more susceptible to HIV infection, thereby explaining the vast prevalence of HIV infection among endemic drug use populations.

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Section: Infection Of Cem X174 Cells With Sivmac239 or Srv-methodsmentioning

confidence: 99%

Morphine Induces Gene Expression of CCR5 in Human CEM x174 Lymphocytes

Miyagi¹,

Chuang²,

Doi³

et al. 2000

Journal of Biological Chemistry

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“…Opioid administration can cause inhibitory effects on antibody and cellular immune responses, natural killer cell activity, cytokine expression and phagocytic activity. The immunologic effects of opioids are mediated by central, as well as peripheral, mechanisms [83][84][85]. The potential by which central opioid receptors mediate peripheral immuno suppression may involve the hypothalamic-pituitary-adrenal axis and the autonomic nervous system.…”

Section: Opioid-induced Immunologic Effectsmentioning

confidence: 99%

“…Interestingly, peripheral immune cells under the influence of cytokines may release endogenous opioids modulating analgesia and inflammatory response. Furthermore, the same cells can express opioid receptors creating a bidirectional system, whereby opioids, immune cells and cytokines dynamically interact [83][84][85]. The central immunologic receptors include µ-opioid receptor, DOR, DOR-antagonist, k-opioid receptor and k-opioid receptor-antagonist [86][87][88].…”

Section: Opioid-induced Immunologic Effectsmentioning

confidence: 99%

Opioids in chronic noncancer pain

Manchikanti

Benyamin

Datta

et al. 2010

Expert Review of Neurotherapeutics

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“…[1][2][3] Furthermore, most leukocytes (monocytes, neutrophils, and T and B lymphocytes) express low levels of mu-opioid receptors and opioid peptides, with a similar pattern of distribution in humans and rodents and opioid receptor levels are markedly induced on activation. 4,5 Although chronic morphine administration has become the gold standard in managing long term pain, it has unwanted side effects, such as respiratory depression, suppression of gastrointestinal motility, and immunosuppression, through its binding to mu opioid receptors on cells in the brainstem, in the gastrointestinal, and on immune cells, poses user complications. 6 -11 Several studies have also documented the process by which wound healing occurs.…”

mentioning

confidence: 99%

Chronic Morphine Administration Delays Wound Healing by Inhibiting Immune Cell Recruitment to the Wound Site

Martin

Koodie

Krishnan

et al. 2010

The American Journal of Pathology

109

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Patients prescribed morphine for the management of chronic pain , and chronic heroin abusers , often present with complications such as increased susceptibility to opportunistic infections and inadequate healing of wounds. We investigated the effect of morphine on wound-healing events in the presence of an infection in an in vivo murine model that mimics the clinical manifestations seen in opioid user and abuser populations. We show for the first time that in the presence of an inflammatory inducer, lipopolysaccharide, chronic morphine treatment results in a marked decrease in wound closure, compromised wound integrity, and increased bacterial sepsis. Morphine treatment resulted in a significant delay and reduction in both neutrophil and macrophage recruitment to the wound site. The delay and reduction in neutrophil reduction was attributed to altered early expression of keratinocyte derived cytokine and was independent of macrophage inflammatory protein 2 expression, whereas suppression of macrophage infiltration was attributed to suppressed levels of the potent macrophage chemoattractant monocyte chemotactic protein-1. When the effects of chronic morphine on later wound healing events were investigated, a significant suppression in angiogenesis and myofibroblast recruitment were observed in animals that received chronic morphine administration. Taken

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Mu Opioid Receptor Gene Expression in Immune Cells

Cited by 181 publications

References 0 publications

Morphine Induces Gene Expression of CCR5 in Human CEM x174 Lymphocytes

Morphine Induces Gene Expression of CCR5 in Human CEM x174 Lymphocytes

Opioids in chronic noncancer pain

Chronic Morphine Administration Delays Wound Healing by Inhibiting Immune Cell Recruitment to the Wound Site

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