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25 results on '"Dabo, Abdoulaye J."'

1. Evaluating Novel Protein Phosphatase 2A Activators as Therapeutics for Emphysema

Author

Soto, Brian, primary, Ahmed, Huma, additional, Pillai, Meshach, additional, Park, Sangmi S, additional, Ploszaj, Magdalena, additional, Reece, Joshua, additional, Taluru, Harsha, additional, Bobrow, Dylan, additional, Yu, Howard, additional, Lafortune, Pascale, additional, Jundi, Bakr, additional, Costanzo, Louis, additional, Dabo, Abdoulaye J., additional, Foronjy, Robert F, additional, Mueller, Christian, additional, Ohlmeyer, Michael, additional, and Geraghty, Patrick, additional

Published
2023
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5. LRP1 loss in airway epithelium exacerbates smoke-induced oxidative damage and airway remodeling

Author

Garcia-Arcos, Itsaso, primary, Park, Sangmi S., additional, Mai, Michelle, additional, Alvarez-Buve, Roger, additional, Chow, Lillian, additional, Cai, Huchong, additional, Baumlin-Schmid, Nathalie, additional, Agudelo, Christina W., additional, Martinez, Jennifer, additional, Kim, Michael D., additional, Dabo, Abdoulaye J., additional, Salathe, Matthias, additional, Goldberg, Ira J., additional, and Foronjy, Robert F., additional

Published
2022
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14. Cigarette Smoke Exposure Reduces Leukemia Inhibitory Factor Levels During Respiratory Syncytial Viral Infection

Author

Poon, Justin, Campos, Michael, Foronjy, Robert F, Nath, Sridesh, Gupta, Gayatri, Railwah, Christopher, Dabo, Abdoulaye J, Baumlin, Nathalie, Salathe, Matthias, and Geraghty, Patrick

Subjects
endocrine system, respiratory syncytial virus, Respiratory Mucosa, Respiratory Syncytial Virus Infections, International Journal of Chronic Obstructive Pulmonary Disease, Cigarette Smoking, chronic obstructive pulmonary disease, Mice, Pulmonary Disease, Chronic Obstructive, Smoke, Tobacco, Animals, Humans, reproductive and urinary physiology, Cells, Cultured, Original Research, lcsh:RC705-779, Inhalation Exposure, cigarette smoke, lcsh:Diseases of the respiratory system, respiratory system, Symptom Flare Up, leukemia inhibitory factor, respiratory tract diseases, 3. Good health, Disease Models, Animal, embryonic structures, Bronchoalveolar Lavage Fluid
Abstract

Justin Poon,1 Michael Campos,2 Robert F Foronjy,1 Sridesh Nath,1 Gayatri Gupta,1 Christopher Railwah,1 Abdoulaye J Dabo,1 Nathalie Baumlin,3 Matthias Salathe,3 Patrick Geraghty11Division of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Medical Center, Brooklyn, NY, USA; 2Division of Pulmonary, Critical Care, and Sleep Medicine, University of Miami, Miami, FL, USA; 3Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS, USABackground: Viral infections are considered a major driving factor of chronic obstructive pulmonary disease (COPD) exacerbations and thus contribute to disease morbidity and mortality. Respiratory syncytial virus (RSV) is a frequently detected pathogen in the respiratory tract of COPD patients during an exacerbation. We previously demonstrated in a murine model that leukemia inhibitory factor (LIF) expression was increased in the lungs during RSV infection. Subduing LIF signaling in this model enhanced lung injury and airway hypersensitivity. In this study, we investigated lung LIF levels in COPD patient samples to determine the impact of disease status and cigarette smoke exposure on LIF expression.Materials and methods: Bronchoalveolar lavage fluid (BALF) was obtained from healthy never smokers, smokers, and COPD patients, by written informed consent. Human bronchial epithelial (HBE) cells were isolated from healthy never smokers and COPD patients, grown at the air–liquid interface and infected with RSV or stimulated with polyinosinic:polycytidylic acid (poly (i:c)). Mice were exposed to cigarette smoke daily for 6 months and were subsequently infected with RSV. LIF expression was profiled in all samples.Results: In human BALF, LIF protein was significantly reduced in both smokers and COPD patients compared to healthy never smokers. HBE cells isolated from COPD patients produced less LIF compared to never smokers during RSV infection or poly (i:c) stimulation. Animals exposed to cigarette smoke had reduced lung levels of LIF and its corresponding receptor, LIFR. Smoke-exposed animals had reduced LIF expression during RSV infection. Two possible factors for reduced LIF levels were increased LIF mRNA instability in COPD epithelia and proteolytic degradation of LIF protein by serine proteases.Conclusions: Cigarette smoke is an important modulator for LIF expression in the lungs. Loss of LIF expression in COPD could contribute to a higher degree of lung injury during virus-associated exacerbations.Keywords: chronic obstructive pulmonary disease, leukemia inhibitory factor, respiratory syncytial virus, cigarette smoke

Published
2019

15. Protein Phosphatase 2A Reduces Cigarette Smoke–induced Cathepsin S and Loss of Lung Function

Author

Doherty, Declan F., primary, Nath, Sridesh, additional, Poon, Justin, additional, Foronjy, Robert F., additional, Ohlmeyer, Michael, additional, Dabo, Abdoulaye J., additional, Salathe, Matthias, additional, Birrell, Mark, additional, Belvisi, Maria, additional, Baumlin, Nathalie, additional, Kim, Michael D., additional, Weldon, Sinéad, additional, Taggart, Clifford, additional, and Geraghty, Patrick, additional

Published
2019
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24. HIV infection model of chronic obstructive pulmonary disease in mice.

Author

Geraghty P, Hadas E, Kim BH, Dabo AJ, Volsky DJ, and Foronjy R

Subjects
Animals, Apoptosis, Disease Models, Animal, Humans, Lung enzymology, Lung immunology, Lung pathology, Lung virology, Macrophages, Alveolar pathology, Macrophages, Alveolar virology, Male, Mice, Neutrophils metabolism, Peptide Hydrolases metabolism, Pneumonia pathology, Smoking adverse effects, HIV Infections complications, Pulmonary Disease, Chronic Obstructive complications
Abstract

Cigarette smoke usage is prevalent in human immunodeficiency virus (HIV)-positive patients, and, despite highly active antiretroviral therapy, these individuals develop an accelerated form of chronic obstructive pulmonary disease (COPD). Studies investigating the mechanisms of COPD development in HIV have been limited by the lack of suitable mouse models. Here we describe a model of HIV-induced COPD in wild-type mice using EcoHIV, a chimeric HIV capable of establishing chronic infection in immunocompetent mice. A/J mice were infected with EcoHIV and subjected to whole body cigarette smoke exposure. EcoHIV was detected in alveolar macrophages of mice. Compared with uninfected mice, concomitant EcoHIV infection significantly reduced forced expiratory flow 50%/forced vital capacity and enhanced distal airspace enlargement following cigarette smoke exposure. Lung IL-6, granulocyte-macrophage colony-stimulating factor, neutrophil elastase, cathepsin G, and matrix metalloproteinase-9 expression was significantly enhanced in smoke-exposed EcoHIV-infected mice. These changes coincided with enhanced IκBα, ERK1/2, p38, and STAT3 phosphorylation and lung cell apoptosis. Thus, the EcoHIV smoke exposure mouse model reproduces several of the pathophysiological features of HIV-related COPD in humans, indicating that this murine model can be used to determine key parameters of HIV-related COPD and to test future therapies for this disorder., (Copyright © 2017 the American Physiological Society.)

Published
2017
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25. TLR9 expression is required for the development of cigarette smoke-induced emphysema in mice.

Author

Foronjy RF, Salathe MA, Dabo AJ, Baumlin N, Cummins N, Eden E, and Geraghty P

Subjects
Adult, Animals, Cells, Cultured, Cytokines biosynthesis, Cytokines genetics, Female, Gene Expression, Humans, Lung pathology, Lung physiopathology, Male, Mice, Inbred C57BL, Middle Aged, Pneumonia etiology, Pneumonia immunology, Pneumonia metabolism, Protein Tyrosine Phosphatase, Non-Receptor Type 1 metabolism, Pulmonary Disease, Chronic Obstructive metabolism, Pulmonary Emphysema etiology, Pulmonary Emphysema immunology, Smoking adverse effects, Toll-Like Receptor 9 biosynthesis, Up-Regulation, Young Adult, Lung metabolism, Pulmonary Emphysema metabolism, Smoke adverse effects, Toll-Like Receptor 9 genetics
Abstract

The expression of Toll-like receptor (TLR)-9, a pathogen recognition receptor that recognizes unmethylated CpG sequences in microbial DNA molecules, is linked to the pathogenesis of several lung diseases. TLR9 expression and signaling was investigated in animal and cell models of chronic obstructive pulmonary disease (COPD). We observed enhanced TLR9 expression in mouse lungs following exposure to cigarette smoke. Tlr9(-/-) mice were resistant to cigarette smoke-induced loss of lung function as determined by mean linear intercept, total lung capacity, lung compliance, and tissue elastance analysis. Tlr9 expression also regulated smoke-mediated immune cell recruitment to the lung; apoptosis; expression of granulocyte-colony stimulating factor (G-CSF), the CXCL5 protein, and matrix metalloproteinase-2 (MMP-2); and protein tyrosine phosphatase 1B (PTP1B) activity in the lung. PTP1B, a phosphatase with anti-inflammatory abilities, was identified as binding to TLR9. In vivo delivery of a TLR9 agonist enhanced TLR9 binding to PTP1B, which inactivated PTP1B. Ptp1b(-/-) mice had elevated lung concentrations of G-CSF, CXCL5, and MMP-2, and tissue expression of type-1 interferon following TLR9 agonist administration, compared with wild-type mice. TLR9 responses were further determined in fully differentiated normal human bronchial epithelial (NHBE) cells isolated from nonsmoker, smoker, and COPD donors, and then cultured at air liquid interface. NHBE cells from smokers and patients with COPD expressed more TLR9 and secreted greater levels of G-CSF, IL-6, CXCL5, IL-1β, and MMP-2 upon TLR9 ligand stimulation compared with cells from nonsmoker donors. Although TLR9 combats infection, our results indicate that TLR9 induction can affect lung function by inactivating PTP1B and upregulating expression of proinflammatory cytokines., (Copyright © 2016 the American Physiological Society.)

Published
2016
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