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Infection and Immunity, October 2009, p. 4597-4608, Vol. 77, No. 10
0019-9567/09/$08.00+0     doi:10.1128/IAI.00212-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Hag Mediates Adherence of Moraxella catarrhalis to Ciliated Human Airway Cells{triangledown} ,§

Rachel Balder,1 Thomas M. Krunkosky,2 Chi Q. Nguyen,1 Lacey Feezel,1 and Eric R. Lafontaine1*

Department of Infectious Diseases, University of Georgia College of Veterinary Medicine, Athens, Georgia 30602,1 Department of Anatomy & Radiology, University of Georgia College of Veterinary Medicine, Athens, Georgia, 306022

Received 24 February 2009/ Returned for modification 16 April 2009/ Accepted 29 July 2009

Moraxella catarrhalis is a human pathogen causing otitis media in infants and respiratory infections in adults, particularly patients with chronic obstructive pulmonary disease. The surface protein Hag (also designated MID) has previously been shown to be a key adherence factor for several epithelial cell lines relevant to pathogenesis by M. catarrhalis, including NCIH292 lung cells, middle ear cells, and A549 type II pneumocytes. In this study, we demonstrate that Hag mediates adherence to air-liquid interface cultures of normal human bronchial epithelium (NHBE) exhibiting mucociliary activity. Immunofluorescent staining and laser scanning confocal microscopy experiments demonstrated that the M. catarrhalis wild-type isolates O35E, O12E, TTA37, V1171, and McGHS1 bind principally to ciliated NHBE cells and that their corresponding hag mutant strains no longer associate with cilia. The hag gene product of M. catarrhalis isolate O35E was expressed in the heterologous genetic background of a nonadherent Haemophilus influenzae strain, and quantitative assays revealed that the adherence of these recombinant bacteria to NHBE cultures was increased 27-fold. These experiments conclusively demonstrate that the hag gene product is responsible for the previously unidentified tropism of M. catarrhalis for ciliated NHBE cells.

* Corresponding author. Mailing address: Riverbend South Research Laboratories, University of Georgia, 220 Riverbend Road Room 146, Athens, GA 30602. Phone: (706) 542-2863. Fax: (706) 542-5771. E-mail: elafon10{at}uga.edu

{triangledown} Published ahead of print on 10 August 2009.

§ Supplemental material for this article may be found at http://iai.asm.org/.

Editor: J. N. Weiser

Infection and Immunity, October 2009, p. 4597-4608, Vol. 77, No. 10
0019-9567/09/$08.00+0     doi:10.1128/IAI.00212-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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