A5057650635- HIV Research and Treatment
- Neuroinflammation and Neurodegeneration Mechanisms
- Chemokine receptors and signaling
- Immune Response and Inflammation
- interferon and immune responses
- Cell Adhesion Molecules Research
- Immune cells in cancer
- Atherosclerosis and Cardiovascular Diseases
- HIV-related health complications and treatments
- RNA regulation and disease
- Immune Cell Function and Interaction
- RNA Interference and Gene Delivery
- Tryptophan and brain disorders
- Monoclonal and Polyclonal Antibodies Research
- Mosquito-borne diseases and control
- HIV/AIDS Research and Interventions
- Barrier Structure and Function Studies
- Immunotherapy and Immune Responses
- Alzheimer's disease research and treatments
- Reproductive System and Pregnancy
- Neuropeptides and Animal Physiology
- Connexins and lens biology
- Cytomegalovirus and herpesvirus research
- Trypanosoma species research and implications
- Autophagy in Disease and Therapy
Albert Einstein College of Medicine
2016-2025
Montefiore Medical Center
1992-2021
Universidad de Los Andes, Chile
2017
Icahn School of Medicine at Mount Sinai
2000-2014
University of Illinois Chicago
2014
Yeshiva University
1994-2011
Hospital for Tropical Diseases
2007
Bipar
1998-2004
Experimental Station
2001
DuPont (United States)
2001
As part of a study on the role cytokines in central nervous system development and dysfunction, we determined pattern cytokine production highly purified cultures microglia astrocytes isolated from second-trimester human fetal brains. Levels TNF-alpha, IL-1 beta, IL-6 mRNA protein were by Northern blot analysis ELISA before after stimulation with LPS, or beta. In microglia, LPS induced for all three cytokines. High levels TNF-alpha also found medium, whereas beta was mostly cell associated....
Encephalitis and dementia associated with acquired immunodeficiency syndrome (AIDS) are characterized by leukocyte infiltration into the CNS, microglia activation, aberrant chemokine expression, blood-brain barrier (BBB) disruption, eventual loss of neurons. Little is known about whether human virus 1 (HIV-1) infection leukocytes affects their ability to transmigrate in response chemokines alter BBB integrity. We now demonstrate that HIV results increased transmigration across our tissue...
HIV infection of the CNS is an early event after primary infection, resulting in neurological complications a significant number individuals despite antiretroviral therapy (ART). The main cells infected with within are macrophages/microglia and small fraction astrocytes. role these few astrocytes pathogenesis neuroAIDS has not been examined extensively. Here, we demonstrate that HIV-infected (4.7 ± 2.8% vitro 8.2 3.9% vivo) compromise blood-brain barrier (BBB) integrity. This BBB disruption...
Vesicles shed from astrocytes after brain trauma trigger hepatic cytokine release to mobilize the peripheral immune response.
Abstract Acquired immunodeficiency syndrome (AIDS)‐associated dementia is often characterized by chronic inflammation, with infected macrophage infiltration of the CNS resulting in production human virus type 1 (HIV‐1) products, including tat, and neurotoxins that contribute to neuronal loss. In addition their established role leukocyte recruitment activation, we identified an additional for chemokines CNS. Monocyte chemoattractant protein‐1 (MCP‐1 or CCL2) regulated upon activation normal T...
AIDS dementia is characterized by neuronal loss in association with synaptic damage. A central predictor for clinical onset of these symptoms the infiltration monocytes and macrophages into CNS parenchyma. Chronic HIV-1 infection also allows cells to serve as reservoirs persistent viral infection. Using a coculture endothelial astrocytes that models several aspects human blood-brain barrier, we examined mechanism whereby HIV-derived factor Tat may facilitate monocyte transmigration. We...
Abstract Monocyte chemoattractant protein-1 (MCP-1) is a member of the chemokine beta family chemoattractants that has been shown to play major role in initiation monocyte and T cell inflammation sites tissue injury. In this study, we have examined distribution MCP-1 expression central nervous system (CNS) associated with autoimmune disease experimental encephalomyelitis (EAE) compared results those detected trauma. EAE, was at onset inflammation, prior clinical disease, lymphocytes...
BACKGROUND Tumor necrosis factor-alpha (TNF alpha), which we and others have shown to be elevated in patients with severe congestive heart failure (CHF), is involved the regulation of nitric oxide metabolism. Whether increased concentrations TNF alpha affect oxide-mediated vasodilation CHF has not been studied previously. METHODS AND RESULTS Serum alpha, interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-6 (IL-6) were determined venous blood (pg/mL) from 17 stable New York Heart...
Abstract We have examined the expression of factors associated with growth, differentiation, and chemotaxis cells monocyte/macrophage series in central nervous system Lewis rats sensitized to develop experimental allergic encephalomyelitis. CSF-1 mRNA increased significantly over that found control animals (sensitized OVA CFA or alone). The elevation levels this growth factor commenced immediately before onset early clinical signs peaked maximal incidence disease. Expression message declined...
HIV infection of the central nervous system can result in neurologic dysfunction with devastating consequences AIDS patients. NeuroAIDS is characterized by neuronal injury and loss, yet there no evidence that infect neurons. Here we show HIV-encoded protein tat triggers formation a macromolecular complex involving low-density lipoprotein receptor-related (LRP), postsynaptic density protein-95 (PSD-95), N -methyl- d -aspartic acid (NMDA) receptors, nitric oxide synthase (nNOS) at plasma...
Abstract In this work, the effects of bacterial LPS, TNF-α, and IFN-γ on gap junctional communication (dye coupling) expression connexin43 (immunofluorescence, immunoblotting, RT-PCR) in monocytes/macrophages were studied. Freshly isolated human monocytes plated at high density treated either with LPS plus or TNF-α became transiently dye coupled (Lucifer yellow) within 24 h. Cells alone remained uncoupled. dye-coupled cells, spread Lucifer yellow to neighboring cells was reversibly blocked...
Abstract TNF-like weak inducer of apoptosis, or TWEAK, is a relatively new member the TNF-ligand superfamily. Ligation TWEAK receptor Fn14 by has proinflammatory effects on fibroblasts, synoviocytes, and endothelial cells. Several TWEAK-inducible cytokines are important in pathogenesis kidney diseases; however, whether can induce effect cells not known. We found that murine mesangial express cell surface receptor. stimulation led to dose-dependent increase CCL2/MCP-1, CCL5/RANTES,...
As HIV infected individuals live longer, the prevalence of associated neurocognitive disorders is increasing, despite successful antiretroviral therapy. CD14(+)CD16(+) monocytes are critical to neuropathogenesis as they promote viral seeding brain and establish neuroinflammation. The mechanisms by which uninfected cross blood barrier enter central nervous system not fully understood. We determined that infection resulted in their highly increased transmigration across response CCL2 compared...
HIV reservoirs persist despite antiretroviral therapy (ART) and are established within a few days after infection. Infected myeloid cells in the central nervous system (CNS) may contribute to establishment of CNS viral reservoir. The mature CD14+ CD16+ monocyte subset enters response chemokines, including CCL2. Entry infected monocytes lead infection other cells, macrophages or microglia astrocytes, release neurotoxic early proteins additional cytokines. This contributes neuroinflammation...
Abstract The migration of leukocytes across the blood-brain barrier (BBB) into central nervous system is critical in pathogenesis inflammatory diseases. production chemokines, such as monocyte-chemoattractant protein-1 (MCP-1), by endothelial cells (EC) and astrocytes may initiate amplify this process. Using a coculture human EC to model BBB, we demonstrated that exogenous MCP-1 induces transmigration monocytes dose-dependent manner. TNF-α, IFN-γ, or IL-1β treatment cocultures also induced...