David L. Goldman
<p>The medical community has long recognized fungi as important allergens for patients with asthma. Interestingly, fungal sensitization is more common in children and has been linked to severe asthma resulting in death. The accepted paradigm is that fungal sensitization occurs as a result of recurrent, transient environmental exposures. Yet, increasing evidence suggests that fungi may interact with people in unrecognized ways to promote asthma. My lab is interested in understanding the role of subclinical fungal infections in asthma and their potential contribution to the high prevalence of asthma in urban areas.<br /><br /></p>
<p><em>Cryptococcus neoformans</em> is an encapsulated fungus that is well suited to serve as co-factor in urban asthma. <em>C. neoformans</em> colonizes pigeon droppings and is endemic to urban areas. Once inhaled, this fungus causes persistent, subclinical infections. We have demonstrated that the majority of Bronx children older than 2 years have serologic evidence of cryptococcal infection. Cryptococcal infection induces TH2 inflammation in animal models. In a rat model, we have shown that cryptococcal pulmonary infection acts a co-factor to enhance allergic inflammation to allergen challenge and promotes airway hyper-responsiveness, both hallmark features of asthma. Pulmonary cryptococcosis also induces chitinase expression, which has recently been implicated as an essential mediator of allergic inflammation.<br /><br /></p>
<p>To study this phenomenon, we have established collaborations with Pulmonary Medicine, Critical Care and Emergency Medicine at the Children’s Hospital of Montefiore. These collaborations provide access to the large number of children with asthma in the Bronx. Current studies underway include a characterization of chitinase expression among asthmatics and a comparison of cryptococcal infection prevalence among asthmatics and non-asthmatics. Animal experimentation directed at understanding the mechanisms and variables related to fungal induced asthma are also underway.<br /><br /></p>
<p>In addition to fungal studies, my lab is interested in anthrax pathogenesis. <em>Bacillus anthracis</em> is widely recognized as a potential agent of bioterrorism as evidenced by the 2001 anthrax attack. The toxins of <em>B. anthracis</em> are essential to virulence. In collaborations with Drs. Arturo Casadevall and Jurgen Brojatsch, we have studied the mechanisms by which <em>Bacillus anthracis</em> toxins contribute to host death. We have identified a previously unrecognized protease in human serum that inactivates the protective antigen component of lethal toxin <em>in vitro</em>. The precise protease and its role in the host response and susceptibility to anthrax remain to be determined. We have also identified a potential role for platelet activating factor (PAF) in mediating the lethal effects of toxin, including the alterations in vascular permeability which is characteristic of anthrax. Together, these observations may have important implications in developing new approaches to the treatment of anthrax.</p>
Dr. Goldman has a special interest in fungal infections in children, including hospital and community acquired mycoses.
Dr. Goldman has two primary research interests: the contribution of fungi to the development of asthma in children and the pathogenesis of C. difficile infection in children
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<p>1. Fungal sensitization in childhood persistent asthma is associated with disease severity. Vicencio AG, Santiago MT, Tsirilakis K, Stone A, Worgall S, Foley EA, Bush D, Goldman DL. Pediatr Pulmonol. 2013 Feb 8. doi: 10.1002/ppul.22779. [Epub ahead of print]</p>
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<p>2. Increased chitinase expression and fungal-specific antibodies in the bronchoalveolar lavage fluid of asthmatic children. Goldman DL, Li X, Tsirilakis K, Andrade C, Casadevall A, Vicencio AG. Clin Exp Allergy. 2012 Apr;42(4):523-30. doi: 10.1111/j.1365-2222.2011.03886.x. Epub 2011 Oct 10.</p>
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<p>3. CHIT1 mutations: genetic risk factor for severe asthma with fungal sensitization? Vicencio AG, Chupp GL, Tsirilakis K, He X, Kessel A, Nandalike K, Veler H, Kipperman S, Young MC, Goldman DL.</p>
<p>Pediatrics. 2010 Oct;126(4):e982-5. doi: 10.1542/peds.2010-0321. Epub 2010 Sep 6.</p>
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<p>4. Proteasome inhibitors prevent caspase-1-mediated disease in rodents challenged with anthrax lethal toxin.Muehlbauer SM, Lima H Jr, Goldman DL, Jacobson LS, Rivera J, Goldberg MF, Palladino MA, Casadevall A, Brojatsch J. Am J Pathol. 2010 Aug;177(2):735-43. doi: 10.2353/ajpath.2010.090828. Epub 2010 Jul 1. Erratum in: Am J Pathol. 2010 Oct;177(4):2145.</p>
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<p>David L. Goldman, MD, is Fellowship Director, Pediatric Infectious Diseases; Associate Professor, Pediatrics, and Associate Professor, Microbiology and Infectious Diseases at Montefiore Einstein. He has a special interest in fungal infections in children, including hospital and community acquired mycoses.</p><p>After earning his Bachelor of Arts from Brandeis University in 1983, Dr. Goldman attended Jefferson Medical College, earning his Doctor of Medicine in 1987. He began his postdoctoral education at St. Vincent’s Hospital. Yale University, New York Medical College, completing a yearlong internship before coming to Einstein’s Jacobi Medical Center, where he completed a residency in pediatrics in 1991, a fellowship in academic pediatrics in 1992 and a fellowship in pediatric infectious diseases in 1996.</p><p>Dr. Goldman has two primary research interests: the contribution of fungi to the development of asthma in children and the pathogenesis of C. difficile infection in children. He has shared his work through conferences, symposia, books, peer-reviewed journals, review articles, abstracts and poster presentations. He has also been an ad hoc reviewer for several journals including <em>Infection and Immunity, Microbes and Infection</em>, and <em>Medical Mycology</em>.</p><p>Dr. Goldman is board certified in pediatrics and pediatric infectious diseases. He is a member of the American Society of Microbiology, the Infectious Diseases Society of America and the Pediatric Infectious Diseases Society.</p>
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