J. Y. Cho

University of California, San Diego, San Diego, CA, United States

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Publications (5)21.74 Total impact

  • Journal of Allergy and Clinical Immunology - J ALLERG CLIN IMMUNOL. 01/2006; 117(2).
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    ABSTRACT: RationaleAirways of patients with fatal asthma are edematous and contain increased vasculature. Recent reports have demonstrated that there is increased expression of proangiogenic cytokines in patients with untreated asthma as well as increased expression of anti-angiogenic molecules in patients who have controlled asthma.
    Journal of Allergy and Clinical Immunology - J ALLERG CLIN IMMUNOL. 01/2004; 113(2).
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    ABSTRACT: Immunostimulatory DNA sequences (ISS) activate the innate immune system to generate antiviral cytokines, such as IFN-gamma. This study investigated whether ISS could reduce viral load, mucus secretion, airway inflammation, and airway hyperreactivity to methacholine in a mouse model of respiratory syncytial virus (RSV) infection. Mice were pretreated with ISS 6 days before RSV infection, and lung indices of RSV viral load (viral titer and PCR), bronchoalveolar lavage fluid cytokines (IFN-gamma), airway inflammation (peribronchial inflammation and periodic acid-Schiff-positive mucus cells), and airway hyperreactivity (methacholine responsiveness) were assessed 4 to 6 days after RSV infection. ISS induced the expression of the antiviral cytokine IFN-gamma in the lung, and this was associated with significantly reduced RSV viral titers, mucus secretion, and peribronchial inflammation. ISS reduced, but did not significantly inhibit, RSV-induced airway hyperreactivity to methacholine. Because ISS induced significant levels of lung IFN-gamma, an immunization strategy based solely on the administration of IFN-gamma may be insufficient to inhibit RSV-induced airway hyperreactivity to methacholine, an endpoint important in the subset of RSV-infected subjects with asthma.
    Journal of Allergy and Clinical Immunology 12/2001; 108(5):697-702. · 12.05 Impact Factor
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    ABSTRACT: Platelet endothelial cell adhesion molecule (PECAM or CD31) is a cell adhesion molecule expressed on circulating leukocytes and endothelial cells that plays an important role in mediating neutrophil and monocyte transendothelial migration in vivo. In this study, we investigated whether eosinophils, like neutrophils and monocytes, utilize PECAM for tissue recruitment to sites of allergic inflammation in vivo. Eosinophils express similar levels of PECAM as neutrophils as assessed by FACS analysis. RT-PCR studies demonstrate that eosinophils like neutrophils express the six extracellular domains of PECAM. Eosinophils exhibit homophilic binding to recombinant PECAM as assessed in a single-cell micropipette adhesion assay able to measure the biophysical strength of adhesion of eosinophils to recombinant PECAM. The strength of eosinophil adhesion to recombinant PECAM is the same as that of neutrophil binding to recombinant PECAM and can be inhibited with an anti-PECAM Ab. Although eosinophils express functional PECAM, anti-PECAM Abs did not inhibit bronchoalveolar lavage eosinophilia, lung eosinophilia, and airway hyperreactivity to methacholine in a mouse model of OVA-induced asthma in vivo. Thus, in contrast to studies that have demonstrated that neutrophil and monocyte tissue recruitment is PECAM dependent, these studies demonstrate that eosinophil tissue recruitment in vivo in this model is PECAM independent.
    The Journal of Immunology 09/2001; 167(4):2292-7. · 5.52 Impact Factor
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    ABSTRACT: Conclusion A variety of DNA-based methods of modulating the immune and/or inflammatory response in animal models of asthma have shown significant promise. Antisense strategies seek to inhibit expression of specific host genes, whereas DNA vaccines aim to modulate the immune response to specific encoded allergens. In contrast, ISS DNA therapy seeks to redirect the host immune response from a Th2 to a Th1 response. Current human studies will help to determine which, if any, of these DNA based therapies is a safe and effective therapy for human asthma.
    Springer Seminars in Immunopathology 02/2000; 22(1-2):117-24. · 4.17 Impact Factor