Effect of Morphine Sulfate on Neonatal Neutrophil Chemotaxis

Yossuck, Panitan; Nightengale, Barbara J.; Fortney, Jim E.; Gibson, Laura F.

doi:10.1097/ajp.0b013e3181582c76

Cited by 26 publications

(11 citation statements)

References 48 publications

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“…For example, compared with older children and adults, neutrophils in the neonatal period have impaired chemotaxis and bactericidal activity [4,5], and T-cell regeneration following intensive chemotherapy, both in number and T-cell repertoire, critically depends on the age of the patient [6]. It is therefore not surprising that the epidemiology of IFI differs between children and adults.…”

Section: Populations At Risk and Epidemiology Of Pediatric Fungal Infecmentioning

confidence: 97%

Invasive fungal infections in the pediatric population

Lehrnbecher

Groll

2011

Expert Review of Anti-infective Therapy

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Section: Populations At Risk and Epidemiology Of Pediatric Fungal Infecmentioning

confidence: 97%

Invasive fungal infections in the pediatric population

Lehrnbecher

Groll

2011

Expert Review of Anti-infective Therapy

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“…A growing body of literature supports morphine’s suppressive effects on recruitment and activation of neutrophils during an innate immune response. Exogenous opioid treatment of human blood neutrophils leads to inhibition of IL-8 production (Glattard et al, 2010), IL-8 receptor expression (Yossuck et al, 2008) as well as IL-8-induced chemotaxis (Grimm et al, 1998b). Similar to human models, murine models of opioid abuse show dose dependent inhibition of neutrophil migration into peri-incisional tissue as determined by myeloperoxidase (MPO) assay and immunohistochemistry (Clark et al, 2007).…”

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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“…Thus morphine might have direct effects on neutrophil cytokine production. In addition to direct effects on neutrophil cytokine production, opioids can also affect neutrophil migration into wounded tissue (Choi et al, 1999; Miyagi et al, 2000; Wang et al, 2005; Yossuck et al, 2008). However the dose required morphine for inhibiting neutrophil migration are far in excess of those required to significantly reduce wound area cytokine levels (Clark et al, 2007).…”

Section: Opioids and Wound Healingmentioning

confidence: 99%

Peripheral mechanisms of pain and analgesia

Stein

Clark

et al. 2009

Brain Research Reviews

237

206

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This review summarizes recent findings on peripheral mechanisms underlying the generation and inhibition of pain. The focus is on events occurring in peripheral injured tissues that lead to the sensitization and excitation of primary afferent neurons, and on the modulation of such mechanisms. Primary afferent neurons are of particular interest from a therapeutic perspective because they are the initial generator of noxious impulses traveling towards relay stations in the spinal cord and the brain. Thus, if one finds ways to inhibit the sensitization and/or excitation of peripheral sensory neurons, subsequent central events such as wind-up, sensitization and plasticity may be prevented. Most importantly, if agents are found that selectively modulate primary afferent function and do not cross the blood-brain-barrier, centrally mediated untoward side effects of conventional analgesics (e.g. opioids, anticonvulsants) may be avoided. This article begins with the peripheral actions of opioids, turns to a discussion of the effects of adrenergic co-adjuvants, and then moves on to a discussion of pro-inflammatory mechanisms focusing on TRP channels and nerve growth factor, their signaling pathways and arising therapeutic perspectives.

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Effect of Morphine Sulfate on Neonatal Neutrophil Chemotaxis

Abstract: Newborn neutrophils had reduced chemotaxis toward IL-8. Exposure to morphine sulfate further decreased their chemotactic function. The differential effect may be explained in part by the reduction of IL-8 receptors of newborn neutrophils after morphine exposure.

Cited by 26 publications

References 48 publications

Invasive fungal infections in the pediatric population

Invasive fungal infections in the pediatric population

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

Peripheral mechanisms of pain and analgesia

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