Slowed Reaction Time in HIV-1-Seropositive Intravenous Drug Users without AIDS

Ayuso-Mateos, José Luís; Pereda, A.; Barrio, Andrés Gómez del; Echevarría, S.; Fariñas, M C; García-Palomo, Daniel

doi:10.1159/000008200

Cited by 14 publications

(7 citation statements)

References 21 publications

(23 reference statements)

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“…DSCG is a compound that inhibits the release of mediators from mast cells and acts as an anti-inflammatory agent [19]. The mechanism of action is not fully understood, but it is probably mediated by the phosphorylation of a 78-kDa mast cell protein, which leads to positional rearrangements of the membrane cytoskeleton and approaches plasma and secretory granule membranes [20].…”

Section: Discussionmentioning

confidence: 99%

Prevention of Mast Cell Degranulation by Disodium Cromoglycate Attenuates the Development of Hypoxic Pulmonary Hypertension in Rats Exposed to Chronic Hypoxia

Baňasová¹,

Maxová

Hampl³

et al. 2008

Respiration

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Background: Chronic hypoxia induces lung vascular remodeling, which results in pulmonary hypertension. Vascular remodeling is associated with collagenolysis and activation of matrix metalloproteinases (MMPs). One of the possible sources of MMPs in hypoxic lung are mast cells. Objective: The role of lung mast cell collagenolytic activity in hypoxic pulmonary hypertension was tested by the inhibitor of mast cell degranulation disodium cromoglycate (DSCG). Methods: Rats were treated with DSCG in an early or later phase of isobaric hypoxia. Control groups were exposed to hypoxia only or to normoxia. Lung hemodynamics, muscularization and collagen metabolism in the walls of peripheral pulmonary vessels in the lungs were measured. Results: DSCG applied at an early phase of exposure to hypoxia reduced the development of pulmonary hypertension, inhibited muscularization in peripheral pulmonary arteries and decreased the amount of collagen cleavage fragments in prealveolar vessels. Conclusions: Mast cell degranulation plays a role in the initiation of hypoxic pulmonary vascular remodeling.

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Section: Discussionmentioning

confidence: 99%

Prevention of Mast Cell Degranulation by Disodium Cromoglycate Attenuates the Development of Hypoxic Pulmonary Hypertension in Rats Exposed to Chronic Hypoxia

Baňasová¹,

Maxová

Hampl³

et al. 2008

Respiration

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“…Although effective HAART therapy significantly reduces systemic viral load, there is no effective therapy for HIV-1 associated neurocognitive disorder (HAND) and more significantly the lifetime prevalence of HAND seems to be on the rise (Kopnisky et al, 2007). Chronic drug users account for approximately a third of all cases of AIDS in the USA and recent data indicate that progression to AIDS associated dementia is markedly accelerated in this population (Hauser et al, 2006; Royal et al, 2003; Ayuso-Mateos et al, 2000; Bell et al, 1998a; Nath, 2002); (Shor-Posner, 2000). A frequent occurrence in the HIV positive intravenous (IV) drug abusing population is the incidence of infection with secondary opportunistic pathogens and concurrent bacterial meningitis.…”

Section: Introductionmentioning

confidence: 99%

Morphine Modulation of Toll-Like Receptors in Microglial Cells Potentiates Neuropathogenesis in a HIV-1 Model of Coinfection with Pneumococcal Pneumoniae

Dutta

Krishnan

Meng

et al. 2012

Journal of Neuroscience

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Chronic drug users account for a third of all cases of AIDS in the USA and the progression to AIDS dementia is accelerated in opiate drug abusers. Clinically, microglial activation better correlates with HIV associated neurocognitive disorders (HAND) than productive HIV-1 infection in the CNS. Moreover, pneumococcal pneumonia is the most common opportunistic infection in individuals with HAND. We show that co-infection with S. pneumoniae may be a contributing factor in the increased prevalence of HAND in the opioid dependent population. Till date there have been no studies published implicating the Toll like receptors (TLR) in the neurocognitive disorders associated with Neuroaids in the context of opportunistic infection. Our studies show for the first time, in a morphine dependent model, synergistic increase and activation of TLR expression in the presence of HIV-1 protein TAT and S. pneumoniae with a significant increase in proinflammatory cytokines (IL-6, TNF-α) levels. Furthermore, concurrent increases in reactive oxygen species (ROS) and nitric oxide (NO) production leading to increased Caspase 3 activation are also observed in both murine and human microglial cells. These effects are recapitulated with TLR 2, 4 & 9 cognate ligands (Pam3CSK4, LPS & CpG) and significantly attenuated in TLR 2, 4 knockout mice and TLR2/4 double knockout mice. Thereby, our findings clearly suggest for the first time that activation of TLRs on microglia cells by morphine and TAT in the context of S. pneumoniae infection may be a potential mechanism for the increased prevalence of HAND in HIV infected opioid dependent patients.

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“…44-46 HIV+ opioid users have also evidenced specific neurocognitive deficits, most reliably noted in the domains of attention, information processing, problem solving, working memory, and psychomotor speed. 47-49 These deficits appear to persist even among HIV+ individuals who are asymptomatic 50-52 and among those in methadone maintenance therapy. 53,54 Margolin et al 55 carefully controlled for numerous potential confounds (sociodemographics, medical and psychiatric illnesses), and still found evidence to suggest that long- and short-term heroin and other drug use variables (eg, severity of drug use problems, current methadone use, positive urine toxicology) accounted for variance in neuropsychiatric impairment.…”

Section: Hiv and Co-occurring Substance Usementioning

confidence: 99%

Substance abuse, hepatitis C, and aging in HIV: common cofactors that contribute to neurobehavioral disturbances

Schuster

González

2012

NBHIV

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Although the prevalence of neurocognitive disturbances among individuals with HIV has decreased in recent years, rates of impairment still remain high. This review presents findings from comorbid conditions that may contribute to further neurocognitive impairments in this already vulnerable population. We will focus on three co-factors that have received substantial attention in the neuroAIDS literature: drug use, hepatitis C co-infection (HCV), and aging. All three conditions commonly co-occur with HIV and likely interact with HIV in complex ways. Collectively, the extant literature suggests that drug use, HCV, and aging serve to worsen the neurocognitive profile of HIV through several overlapping mechanisms. A better understanding of how specific comorbidities interact with HIV may reveal specific phenotypes of HIV-associated neurocognitive disorder that may aid in the development of more targeted behavioral and pharmacological treatment efforts.

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Slowed Reaction Time in HIV-1-Seropositive Intravenous Drug Users without AIDS

Cited by 14 publications

References 21 publications

Prevention of Mast Cell Degranulation by Disodium Cromoglycate Attenuates the Development of Hypoxic Pulmonary Hypertension in Rats Exposed to Chronic Hypoxia

Prevention of Mast Cell Degranulation by Disodium Cromoglycate Attenuates the Development of Hypoxic Pulmonary Hypertension in Rats Exposed to Chronic Hypoxia

Morphine Modulation of Toll-Like Receptors in Microglial Cells Potentiates Neuropathogenesis in a HIV-1 Model of Coinfection with Pneumococcal Pneumoniae

Substance abuse, hepatitis C, and aging in HIV: common cofactors that contribute to neurobehavioral disturbances

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