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

Patel, Kalpesh; Bhaskaran, Madhu; Dani, Dhimant; Reddy, Krishna; Singhal, Pravin C.

doi:10.1086/346042

Cited by 36 publications

(29 citation statements)

References 50 publications

(54 reference statements)

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“…In addition, peritoneal macrophages, as well as bone marrow cells harvested from morphine-treated mice, showed decreased migration across the filter of a modified Boyden chamber compared with control cells. Furthermore, morphine promotes HO-1 expression by macrophages, where increased HO-1 activity is associated with decreased macrophage migration [58].…”

Section: Cellular Components and Receptorsmentioning

confidence: 99%

Opiate abuse, innate immunity, and bacterial infectious diseases

Wang

Barke

et al. 2008

Arch. Immunol. Ther. Exp.

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The first line of defense against invading bacteria is provided by the innate immune system. Morphine and other opiates can immediately disrupt the body's first line of defense against harmful external bacteria. Opiate, for example morphine, abuse degrades physical and physiologic barriers, and modulates phagocytic cells (macrophages, neutrophils) and, nonspecific cytotoxic T cells (gammadelta T), natural killer cells, and dendritic cells, that are functionally important for carrying out a rapid immune reaction to invading pathogens. In vitro studies with innate immune cells from experimental animals and humans and in vivo studies with animal models have shown that opiate abuse impairs innate immunity and is responsible for increased susceptibility to bacterial infection. However, to better understand the complex interactions between opiates, innate immunity, and bacterial infection and develop novel approaches to treat and even prevent bacterial infection in the opiate-abuse population, there is an urgent need to fill the numerous gaps in our understanding of the cellular and molecular mechanisms by which opiate abuse increases susceptibility to bacterial infection.

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Section: Cellular Components and Receptorsmentioning

confidence: 99%

Opiate abuse, innate immunity, and bacterial infectious diseases

Wang

Barke

et al. 2008

Arch. Immunol. Ther. Exp.

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“…Moreover, antioxidants and free-radical scavengers prevent morphine-induced GEC growth as well as apoptosis, suggesting that morphine's effects may be mediated through oxidative stress. Morphine stimulates the production of superoxide by macrophages and mesangial cells (187,191), as well as the activity of macrophage heme oxygenase (192), an oxidative stress marker (193). Morphine exerts a bimodal effect on heme oxygenase activity in GEC as well (192), stimulatory at lower and suppressive at higher concentrations.…”

Section: Direct Effects Of Heroin/morphine On the Kidney: Pathophysiomentioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

121

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Renal disease in cocaine and heroin users is associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis, interstitial nephritis, and rhabdomyolysis. The pathophysiologic basis of cocaine-related renal injury involves renal hemodynamic changes, glomerular matrix synthesis and degradation, and oxidative stress and induction of renal atherogenesis. Heroin is the most commonly abused opiate in the United States. Previous studies identified a spectrum of renal diseases in heroin users. The predominant renal lesion in black heroin users is focal segmental glomerulosclerosis and in white heroin users is membranoproliferative glomerulonephritis. Although the prevalence of heroin use in the United States has increased, the incidence of "heroin nephropathy" has declined. Because reports of heroin nephropathy predated the surveillance of hepatitis C virus and HIV, the varied findings might be related to the spectrum of viral illnesses that are encountered in injection drug users. Socioeconomic conditions, cultural and behavioral practices, or differences in genetic susceptibilities may be more associated with the development of nephropathy in heroin users than the drug's pharmacologic properties. Administration of cocaine in animal models results in nonspecific glomerular, interstitial, and tubular cell lesions, but there is no animal model of heroin-associated renal disease. The heterogeneity of responses that are associated with heroin is not consistent with a single or simple notion of nephropathogenesis. There are no well-designed, prospective, epidemiologic studies to assess the incidence and the prevalence of renal disease in populations of opiate users and to establish the validity of a syndrome such as heroin nephropathy. It is concluded although there is a paucity of evidence to support a heroinassociated nephropathy, the evidence from in vitro cellular and animal studies to support the existence of cocaine-induced renal changes is more convincing.

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“…In addition to the hormone-mediated "indirect" modulation of cell proliferation, opioids modify T-and B-cell responses (Guan et al, 1997;Shahabi et al, 2000;Beagles et al, 2004;Roy et al, 2004), macrophage and microglial activity (Belkowski et al, 1995;Hu et al, 2000;Hu et al, 2002), chemotaxis (Szabo et al, 2002), cell migration (Patel et al, 2003), and natural killer cell cytotoxicity (Hsueh et al, 1996;Boyadjieva et al, 2001;Yeager et al, 2002) by modifying cytokine and chemokine release (Belkowski et al, 1995;Alicea et al, 1996;Kong et al, 1997;Wetzel et al, 2000b;Sacerdote, 2003), respective receptor expression (Zhang and Rogers, 2000), and chemokine receptor responsiveness (Grimm et al, 1998a;Rogers et al, 2000;Szabo et al, 2002Szabo et al, , 2003Chen et al, 2004) (for review, see McCarthy et al, 2001 and. These effects do not necessarily affect survival of the opioid-stimulated cell but may modify the course of inflammatory and infectious diseases, such as HIV infection, and thereby survival of the organism.…”

Section: B Chemokine-and Cytokine-mediated Effectsmentioning

confidence: 99%