Browsing by Author "Cohen, Noam A."

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    Inherent differences in nasal and tracheal ciliary function in response to Pseudomonas aeruginosa challenge
    (SAGE PUBLICATIONS INC, 2011) Zhao, Ke Qing; Goldstein, Natalia; Yang, Haibin; Cowan, Andrew T.; Chen, Bei; Zheng, Chunquan; Palmer, James N.; Kreindler, James L.; Cohen, Noam A.
    Background: Sinonasal mucosal biofilms are recognized as contributors to the pathogenesis of chronic rhinosinusitis (CRS). Attachment of bacteria to the sinonasal surface is an initial step in biofilm formation. A critical defense against this occurrence is mucociliary clearance (MCC). To ascertain whether the ciliary component of MCC is uniform throughout the airway we compared ciliary beat frequency (CBF) in the murine nasal septum and trachea at baseline and after challenge with Pseudomonas aeruginosa, a common pathogen of CRS.
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    TNFα Affects Ciliary Beat Response to Increased Viscosity in Human Pediatric Airway Epithelium
    (2016) González, Claudia; Droguett, Karla; Ríos, Mariana; Cohen, Noam A.; Villalón, Manuel J.
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    Tobacco Smoke Mediated Induction of Sinonasal Microbial Biofilms
    (PUBLIC LIBRARY SCIENCE, 2011) Goldstein Daruech, Natalia; Cope, Emily K.; Zhao, Ke Qing; Vukovic, Katarina; Kofonow, Jennifer M.; Doghramji, Laurel; Gonzalez, Bernardo; Chiu, Alexander G.; Kennedy, David W.; Palmer, James N.; Leid, Jeffery G.; Kreindler, James L.; Cohen, Noam A.
    Cigarette smokers and those exposed to second hand smoke are more susceptible to life threatening infection than nonsmokers. While much is known about the devastating effect tobacco exposure has on the human body, less is known about the effect of tobacco smoke on the commensal and commonly found pathogenic bacteria of the human respiratory tract, or human respiratory tract microbiome. Chronic rhinosinusitis (CRS) is a common medical complaint, affecting 16% of the US population with an estimated aggregated cost of $6 billion annually. Epidemiologic studies demonstrate a correlation between tobacco smoke exposure and rhinosinusitis. Although a common cause of CRS has not been defined, bacterial presence within the nasal and paranasal sinuses is assumed to be contributory. Here we demonstrate that repetitive tobacco smoke exposure induces biofilm formation in a diverse set of bacteria isolated from the sinonasal cavities of patients with CRS. Additionally, bacteria isolated from patients with tobacco smoke exposure demonstrate robust in vitro biofilm formation when challenged with tobacco smoke compared to those isolated from smoke naive patients. Lastly, bacteria from smoke exposed patients can revert to a non-biofilm phenotype when grown in the absence of tobacco smoke. These observations support the hypothesis that tobacco exposure induces sinonasal biofilm formation, thereby contributing to the conversion of a transient and medically treatable infection to a persistent and therapeutically recalcitrant condition.