Human neutrophil migration is enhanced by beta-endorphin

Simpkins, Cuthbert O.; Dickey, Cynthia A.; Fink, Mitchell P.

doi:10.1016/0024-3205(84)90213-3

Cited by 64 publications

(16 citation statements)

References 12 publications

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“…Neutrophil chemotaxis in vitro is induced to lesser extent by p-endorphin relative to the effect on the macrophage ( VAN Epps and SALAND 1984;SIMPKINS et al 1984). Neutrophil shape is also affected by p-endorphin.…”

Section: '-Endorphinmentioning

confidence: 95%

Opioids in Immunologic Processes

Bryant¹,

Holaday²

1993

Opioids II

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Section: '-Endorphinmentioning

confidence: 95%

Opioids in Immunologic Processes

Bryant¹,

Holaday²

1993

Opioids II

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“…Interestingly, unlike exogenous opioids, endogenous opioids enhance neutrophil migration through an increase in human neutrophil chemotaxis following endogenous opioid (β-endorphin) treatment (Simpkins et al, 1984). One explanation for the differences between the effects of endogenous and exogenous opioids on neutrophil recruitment may in part be explained by the differences in affinity of morphine and β-endorphins for the mu opioid receptors on immune cells.…”

Section: Morphine Modulation Of Innate Immune Functionmentioning

confidence: 99%

Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections

Roy

Ninković

Banerjee

et al. 2011

J Neuroimmune Pharmacol

267

228

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Infection rate among intravenous drug users (IDU) is higher than the general public, and is the major cause of morbidity and hospitalization in the IDU population. Epidemiologic studies provide data on increased prevalence of opportunistic bacterial infections such as TB and pneumonia, and viral infections such as HIV-1 and hepatitis in the IDU population. An important component in the intravenous drug abuse population and in patients receiving medically indicated chronic opioid treatment is opioid withdrawal. Data on bacterial virulence in the context of opioid withdrawal suggest that mice undergoing withdrawal had shortened survival and increased bacterial load in response to Salmonella infection. As the body of evidence in support of opioid dependency and its immunosuppressive effects is growing, it is imperative to understand the mechanisms by which opioids exert these effects and identify the populations at risk that would benefit the most from the interventions to counteract opioid immunosuppressive effects. Thus, it is important to refine the existing animal model to closely match human conditions and to cross-validate these findings through carefully controlled human studies. Better understanding of the mechanisms will facilitate the search for new therapeutic modalities to counteract adverse effects including increased infection rates. This review will summarize the effects of morphine on innate and adaptive immunity, identify the role of the mu opioid receptor in these functions and the signal transduction activated in the process. The role of opioid withdrawal in immunosuppression and the clinical relevance of these findings will also be discussed.

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“…Exogenous opioid treatment of peripheral human blood neutrophils leads to inhibition of IL-8-induced chemotaxis (Grimm et al, 1998a). Conversely, Simpkins et al reported an increase in neutrophil chemotaxis following endogenous opioid (β-endorphin) treatment (Simpkins et al, 1984). The discrepancy of the latter finding may in part be explained by the differences in affinity of morphine and β-endorphins to the mu-opioid receptors on immune cells.…”

Section: Opioid Modulation Of Immune Cell Functionmentioning

confidence: 99%

Role of the mu-opioid receptor in opioid modulation of immune function

2011

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SUMMARY Endogenous opioids are synthesized in vivo in order to modulate pain mechanisms and inflammatory pathways. Endogenous and exogenous opioids mediate analgesia in response to painful stimuli by binding to opioid receptors on neuronal cells. However, wide distribution of opioid receptors on tissues and organ systems outside the CNS, such as the cells of the immune system, indicate that opioids are capable of exerting additional effects in the periphery, such as immunomodulation. The increased prevalence of infections in opioid abusers based epidemiological studies further highlights the immunosuppressive effects of opioids. In spite of their many debilitating side effects, prescription opioids remain a gold standard for treatment of chronic pain. Therefore, given the prevalence of opioid use and abuse, opioid mediated immune suppression presents a serious concern in our society today. It is imperative to understand the mechanisms by which exogenous opioids modulate immune processes. In this review we will discuss the role of opioid receptors and their ligands in mediating immune suppressive functions. We will summarize recent studies on direct and indirect opioid modulation of the cells of the immune system as well as the role of opioids in exacerbation of certain disease states.

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Human neutrophil migration is enhanced by beta-endorphin

Cited by 64 publications

References 12 publications

Opioids in Immunologic Processes

Opioids in Immunologic Processes

Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections

Role of the mu-opioid receptor in opioid modulation of immune function

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