Drug abuse and neuropathogenesis of HIV infection: role of DC-SIGN and IDO

Nair, Madhavan; Schwartz, Stanley A.; Mahajan, Supriya D.; Tsiao, Chubin; Chawda, Ram; Whitney, Robert B.; Sykes, Bindukumar B. Don; Hewitt, Ross G.

doi:10.1016/j.jneuroim.2004.08.040

Cited by 26 publications

(26 citation statements)

References 30 publications

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“…These bDC could respond to signals from the milieu during this stage of development that induce such basic functions as phagocytosis and removal of cell debris. Likewise, the EYFP ϩ bDC might maintain a developmental residual function in the adult CNS, as others have postulated for the "microglia," and be involved in synaptic plasticity and neurogenesis over the life span of the mouse (Cohen et al, 1997;Cohen and Schwartz, 1999;Nair et al, 2004;Kipnis and Schwartz, 2005;Butovsky et al, 2005Butovsky et al, , 2006aSchwartz and Yoles, 2006;Ziv et al, 2006a,b) A possible function for brain DC in neurogenesis is reinforced in the present study by their location in regions well recognized for postnatal neurogenesis and neural remodeling, e.g., the dentate gyrus in the normal adult (Gould and Cameron, 1996) and following seizures (Jessberger et al, 2005), the subventricular zone of the lateral ventricles (Mercier et al, 2002), the olfactory pathways comprising the rostral migratory stream, and within layer II of the piriform cortex (Ramirez-Castillejo et al, 2002). Other studies have suggested a role for microglia in neurogenesis, but none has identified any unique features of these cells that distinguish them from the general "microglia population."…”

Section: Distribution Of Eyfp ؉ Bdc In Embryonic Neonatal and Adultmentioning

confidence: 88%

CD11c/EYFP transgene illuminates a discrete network of dendritic cells within the embryonic, neonatal, adult, and injured mouse brain

Bulloch

Miller

Gal-Toth

et al. 2008

J of Comparative Neurology

195

163

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The CD11c enhanced yellow fluorescent protein (EYFP) transgenic mouse was constructed to identify dendritic cells in the periphery (Lindquist et al. [2004] Nat. Immunol. 5:1243-1250). In this study, we used this mouse to characterize dendritic cells within the CNS. Our anatomic results showed discrete populations of EYFP(+) brain dendritic cells (EYFP(+) bDC) that colocalized with a small fraction of microglia immunoreactive for Mac-1, Iba-1, CD45, and F4/80 but not for NeuN, Dcx, NG2 proteoglycan, or GFAP. EYFP(+) bDC, isolated by fluorescent activated cell sorting (FACS), expressed mRNA for the Itgax (CD11c) gene, whereas FACS anlaysis of EYFP(+) bDC cultures revealed the presence of CD11c protein. Light microscopy studies revealed that EYFP(+) bDC were present in the embryonic CNS when the blood-brain barrier is formed and postnatally when brain cells are amenable to culturing. In adult male mice, EYFP(+) bDC distribution was prominent within regions of the CNS that 1) are subject to structural plasticity and neurogenesis, 2) receive sensory and humoral input from the external environment, and 3) lack a blood-brain barrier. Ultrastructural analysis of EYFP(+) bDC in adult neurogenic niches showed their proximity to developing neurons and a morphology characteristic of immune/microglia cells. Kainic acid-induced seizures revealed that EYFP(+) bDC responded to damage of the hippocampus and displayed morphologies similar to those described for seizure-activated EGFP(+) microglia in the hippocampus of cfms (CSF-1R) EGFP mice. Collectively, these findings suggest a new member of the dendritic cell family residing among the heterogeneous microglia population.

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Section: Distribution Of Eyfp ؉ Bdc In Embryonic Neonatal and Adultmentioning

confidence: 88%

CD11c/EYFP transgene illuminates a discrete network of dendritic cells within the embryonic, neonatal, adult, and injured mouse brain

Bulloch

Miller

Gal-Toth

et al. 2008

J of Comparative Neurology

195

163

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“…What is becoming clear from some data is that the probability of infected leukocyte transmigration across the BBB may be even greater for COC and/or METH abusers than nondrug abusers; as COC and METH have been shown to up-regulate molecules that facilitate transmigration of HIV across the BBB such as MMPs and DC-SIGN (Conant et al, 2004;Nair et al, 2004). Furthermore, research has shown that COC binds to and enters brain microvascular endothelial cells (BMEC), and up-regulates gene transcription important for normal physiological functioning and maintenance of BMECs, thereby disrupting tight junctions and increasing permeability to HIV among other things (Fiala et al, 2005).…”

Section: Hiv + Cocaine And/or Methamphetamine Neurotoxicitymentioning

confidence: 99%

Neurotoxic profiles of HIV, psychostimulant drugs of abuse, and their concerted effect on the brain: Current status of dopamine system vulnerability in NeuroAIDS

Ferris

Mactutus

Booze

2008

Neuroscience & Biobehavioral Reviews

118

131

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There are roughly 30 to 40 million HIV infected individuals in the world as of December 2007, and drug abuse directly contributes to one-third of all HIV-infections in the United States. Antiretroviral therapy has increased the lifespan of HIV-seropositives, but CNS function often remains diminished, effectively decreasing quality of life. A modest proportion may develop HIV-associated dementia, the severity and progression of which is increased with drug abuse. HIV and drugs of abuse in the CNS target subcortical brain structures and DA systems in particular. This toxicity is mediated by a number of neurotoxic mechanisms, including but not limited to, aberrant immune response and oxidative stress. Therefore, novel therapeutic strategies must be developed that can address a wide variety of disparate neurotoxic mechanisms and apoptotic cascades. This paper reviews the research pertaining to the where, what, and how of HIV and cocaine/methamphetamine toxicity in the CNS. Specifically, where these toxins most affect the brain, what aspects of the virus are neurotoxic, and how these toxins mediate neurotoxicity.

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“…NHA were treated with and without cocaine-hydrochloride (Sigma-Aldrich, St. Louis MO); time and concentration used were based on previous studies that produced a maximum biological response without causing toxicity to the target cells (Nair et al, 2000;Nair et al, 2001;Nair et al, 2004;Nair et al, 2005). Cocaine was dissolved in sterile distilled water and was subsequently diluted in media to the required concentrations.…”

Section: Drug Treatmentmentioning

confidence: 99%

Proteomic analysis of the effects of cocaine on the enhancement of HIV-1 replication in normal human astrocytes (NHA)

et al. 2006

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The US is experiencing an epidemic of cocaine use entangled with HIV-1 infection. Normal human astrocytes (NHA) are susceptible to HIV-1 infection. We utilized LTR-R/U5 amplification, p24 antigen assay and the proteomic method of difference gel electrophoresis (DIGE) combined with protein identification through HPLC-MS/MS to investigate the effect of cocaine on HIV-1 infectivity and the proteomic profile of NHA, respectively. Data demonstrate that cocaine significantly upregulates HIV-1 infection in NHA as measured by LTR-R/U5 amplification and p24 antigen assay. Further, our results show for the first time that cocaine differentially regulates the expression of a number of proteins by NHA that may play a role in the neuropathogenesis of HIV-1 disease.

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Drug abuse and neuropathogenesis of HIV infection: role of DC-SIGN and IDO

Cited by 26 publications

References 30 publications

CD11c/EYFP transgene illuminates a discrete network of dendritic cells within the embryonic, neonatal, adult, and injured mouse brain

CD11c/EYFP transgene illuminates a discrete network of dendritic cells within the embryonic, neonatal, adult, and injured mouse brain

Neurotoxic profiles of HIV, psychostimulant drugs of abuse, and their concerted effect on the brain: Current status of dopamine system vulnerability in NeuroAIDS

Proteomic analysis of the effects of cocaine on the enhancement of HIV-1 replication in normal human astrocytes (NHA)

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