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Lisa Ryan   Dr.  Institute, Department or Faculty Head 
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Lisa Ryan published an article in August 2018.
Top co-authors See all
Gill Diamond

51 shared publications

Department of Oral Biology, University of Florida, Gainesville, Florida

Kartikeya Cherabuddi

19 shared publications

University of Florida College of Medicine, Gainesville, Florida

Jeffry C. Pelletier

8 shared publications

Fox Chase Chemical Diversity Center, Inc., 3805 Old Easton Road, Doylestown, Pennsylvania 18902, United States

Richard W. Scott

4 shared publications

Fox Chase Chemical Diversity Center, Doylestown, PA 18902, USA

Lisa Kathleen Ryan

3 shared publications

The Public Health Research Institute Center, Rutgers New Jersey Medical School, Newark, NJ 07103, USA

Publication Record
Distribution of Articles published per year 

Total number of journals
published in
Article 0 Reads 0 Citations β-Defensins Coordinate In Vivo to Inhibit Bacterial Infections of the Trachea Lisa Kathleen Ryan, Jichuan Wu, Kyell Schwartz, Sunghan Yim,... Published: 28 August 2018
Vaccines, doi: 10.3390/vaccines6030057
DOI See at publisher website PubMed View at PubMed ABS Show/hide abstract
β-defensins are predicted to play an important role in innate immunity against bacterial infections in the airway. We previously observed that a type III-secretion product of Bordetella bronchiseptica inhibits the NF-κB-mediated induction of a β-defensin in airway epithelial cells in vitro. To confirm this in vivo and to examine the relative roles of other β-defensins in the airway, we infected wild-type C57BL/6 mice and mice with a deletion of the mBD-1 gene with B. bronchiseptica wild-type strain, RB50 and its mutant strain lacking the type III-secretion system, WD3. The bacteria were quantified in the trachea and the nasal tissue and mRNA levels of mouse β-defensin-3 (mBD-3) were assessed after 24 h. Infection with the wild-type bacterial strain resulted in lower mBD-3 mRNA levels in the trachea than in mice infected with the type III-deficient strain. Furthermore, we observed an increase in bacterial numbers of RB50 only in the tracheas of mBD-1-deficient mice. Neutrophils were also more abundant on the trachea in RB50 infected WT mice but not in the bronchiolar lavage fluid (BAL), compared with WD3 infected WT and mBD-1−/− mice, indicating that the coordination of β-defensin chemotactic effects may be confined to tracheal epithelial cells (TEC). RB50 decreased the ability of mice to mount an early specific antibody response, seven days after infection in both WT and mBD-1−/− mice but there were no differences in titers between RB50-infected WT and mBD-1−/− mice or between WD3-infected WT and mBD-1−/− mice, indicating mBD-1 was not involved in induction of the humoral immune response to the B. bronchiseptica. Challenge of primary mouse TEC in vitro with RB50 and WD3, along with IL-1β, further corroborated the in vivo studies. The results demonstrate that at least two β-defensins can coordinate early in an infection to limit the growth of bacteria in the trachea.
Article 1 Read 0 Citations Antifungal Potential of Host Defense Peptide Mimetics in a Mouse Model of Disseminated Candidiasis Mobaswar Hossain Chowdhury, Lisa Kathleen Ryan, Kartikeya Ch... Published: 27 February 2018
Journal of Fungi, doi: 10.3390/jof4010030
DOI See at publisher website PubMed View at PubMed ABS Show/hide abstract
Invasive candidiasis caused by Candida albicans and non-albicans Candida (NAC) present a serious disease threat. Although the echinocandins are recommended as the first line of antifungal drug class, resistance to these agents is beginning to emerge, demonstrating the need for new antifungal agents. Host defense peptides (HDP) exhibit potent antifungal activity, but as drugs they are difficult to manufacture efficiently, and they are often inactivated by serum proteins. HDP mimetics are low molecular weight non-peptide compounds that can alleviate these problems and were shown to be membrane-active against C. albicans and NAC. Here, we expand upon our previous works to describe the in vitro and in vivo activity of 11 new HDP mimetics that are active against C. albicans and NAC that are both sensitive and resistant to standard antifungal drugs. These compounds exhibit minimum inhibitory/fungicidal concentration (MIC/MFC) in the µg/mL range in the presence of serum and are inhibited by divalent cations. Rapid propidium iodide influx into the yeast cells following in vitro exposure suggested that these HDP mimetics were also membrane active. The lead compounds were able to kill C. albicans in an invasive candidiasis CD-1 mouse model with some mimetic candidates decreasing kidney burden by 3–4 logs after 24 h in a dose-dependent manner. The data encouraged further development of this new anti-fungal drug class for invasive candidiasis.
Article 0 Reads 2 Citations Modulation of Human β-Defensin-1 Production by Viruses Lisa Kathleen Ryan, Gill Diamond, Theresa Li-Yun Chang Published: 21 June 2017
Viruses, doi: 10.3390/v9060153
DOI See at publisher website PubMed View at PubMed ABS Show/hide abstract
While initially identified as a broad-spectrum antimicrobial peptide, constitutively expressed in epithelia, human β-defensin (hBD)-1 is now recognized to have a more complex pattern of expression of its gene, DEFB1, as well as activities that extend beyond direct antimicrobial. These observations suggest a complex role for hBD-1 in the host defense against viral infections, as evidenced by its expression in cells involved in viral defense, and its gene regulation in response to viral challenge. This regulation is observed both in vitro and in vivo in humans, as well as with the murine homolog, mBD-1. While numerous reviews have summarized the existing literature on β-defensin gene expression and activity, here we provide a focused review of relevant studies on the virus-mediated regulation of hBD-1 and how this regulation can provide a crucial aspect of the innate immune defense against viral infection.