Severe Systemic Infections Complicating "Mainline" Heroin Addiction

Briggs, James

doi:10.1016/s0140-6736(67)90565-x

Cited by 87 publications

(13 citation statements)

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“…In 1967 three separate reports were made which described the increase in incidence of a number of bacterial and viral infections in heroin addicts (BRIGGS et al 1967;CHERUBIN 1967;Lou RIA et al 1967) including: bacterial endocarditis, tetanus, various pulmonary infections, sepsis, malaria, and hepatitis. Obviously a number of factors in addition to potential immunosuppressive effects of heroin could account for these phenomena.…”

Section: Other Opioidsmentioning

confidence: 99%

Opioids in Immunologic Processes

Bryant¹,

Holaday²

1993

Opioids II

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Section: Other Opioidsmentioning

confidence: 99%

Opioids in Immunologic Processes

Bryant¹,

Holaday²

1993

Opioids II

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“…The increased incidence of infection was once attributed to the use of nonsterile and contaminated needles by drug addicts. Other investigators have emphasized the role of impurities in street heroin [3,4]. Because mononuclear phagocytes have been demonstrated to possess opiate receptors, the direct effect of opiates on these cells is increasingly recognized [5][6][7][8].…”

mentioning

confidence: 99%

Role of Heme Oxygenase–1 in Morphine‐Modulated Apoptosis and Migration of Macrophages

Patel¹,

Bhaskaran²,

Dani³

et al. 2003

J INFECT DIS

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We examined the role of heme oxygenase (HO)-1 in morphine-induced decrease in macrophage migration. Morphine promoted expression of HO-1 in murine macrophages. Morphine-receiving mice (MRCs) showed decreased (P<.001) macrophage migration and increased (P<.001) occurrence of macrophage apoptosis. In in vitro studies, peritoneal macrophages harvested from MRCs also showed decreased (P<.001) migration, compared with those from control mice. Bone marrow cells isolated from MRCs showed not only decreased (P<.001) migration but also increased apoptosis. Pretreatment of MRCs with hemin not only decreased migration of macrophages further but also enhanced the apoptosis of peritoneal macrophages. On the other hand, pretreatment of MRCs with zinc protoporphyrin attenuated the effect of morphine on both macrophage migration and the occurrence of apoptosis. In in vitro studies, pretreatment of macrophages with hemin exacerbated morphine-induced apoptosis, whereas pretreatment with zinc protoporphyrin attenuated morphine-induced macrophage apoptosis.

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“…Opiate addicts are prone to bacterial infections (1)(2)(3)(4). Because the mononuclear phagocyte system plays a critical role in the host's defense against bacteria, modulation of monocyte function by morphine may be important.…”

mentioning

confidence: 99%

Role of P38 Mitogen-Activated Protein Kinase Phosphorylation and Fas-Fas Ligand Interaction in Morphine-Induced Macrophage Apoptosis

Singhal

Bhaskaran

Patel

et al. 2002

The Journal of Immunology

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In this study, we evaluated the molecular mechanisms involved in morphine-induced macrophage apoptosis. Both morphine and TGF-β promoted P38 mitogen-activated protein kinase (MAPK) phosphorylation, and this phosphorylation was inhibited by SB 202190 as well as by SB 203580. Anti-TGF-β Ab as well as naltrexone (an opiate receptor antagonist) inhibited morphine-induced macrophage P38 MAPK phosphorylation. Anti-TGF-β Ab also attenuated morphine-induced p53 as well as inducible NO synthase expression; in contrast, NG-nitro-l-arginine methyl ester, an inhibitor of NO synthase, inhibited morphine-induced P38 MAPK phosphorylation and Bax expression. Morphine also enhanced the expression of both Fas and Fas ligand (FasL), whereas anti-FasL Ab prevented morphine-induced macrophage apoptosis. Moreover, naltrexone inhibited morphine-induced FasL expression. In addition, macrophages either deficient in FasL or lacking p53 showed resistance to the effect of morphine. Inhibitors of both caspase-8 and caspase-9 partially prevented the apoptotic effect of morphine on macrophages. In addition, caspase-3 inhibitor prevented morphine-induced macrophage apoptosis. These findings suggest that morphine-induced macrophage apoptosis proceeds through opiate receptors via P38 MAPK phosphorylation. Both TGF-β and inducible NO synthase play an important role in morphine-induced downstream signaling, which seems to activate proteins involved in both extrinsic (Fas and FasL) and intrinsic (p53 and Bax) cell death pathways.

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Severe Systemic Infections Complicating "Mainline" Heroin Addiction

Cited by 87 publications

References 0 publications

Opioids in Immunologic Processes

Opioids in Immunologic Processes

Role of Heme Oxygenase–1 in Morphine‐Modulated Apoptosis and Migration of Macrophages

Role of P38 Mitogen-Activated Protein Kinase Phosphorylation and Fas-Fas Ligand Interaction in Morphine-Induced Macrophage Apoptosis

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