Published ahead of print on May 4, 2006, doi:10.1164/rccm.200509-1459OC Am. J. Respir. Crit. Care Med., Volume 174, Number 2, July 2006, 213-220 A more recent version of this article appeared on July 15, 2006
Submitted on September 19, 2005 Haemophilus influenzae Forms Biofilms on Airway Epithelia: Implications in Cystic FibrosisTimothy D Starner1*,1 Department of Pediatrics, The University of Iowa, Iowa City, Iowa, USA, 2 Department of Microbiology, The University of Iowa, Iowa City, Iowa, USA * To whom correspondence should be addressed. E-mail: timothy-starner{at}uiowa.edu.
Rationale: Non-typeable Haemophilus influenzae (NTHi) commonly infects patients with cystic fibrosis (CF), especially early in childhood. Bacteria biofilms are increasingly recognized as contributing to bacterial persistence and disease pathogenesis in cystic fibrosis.
Objectives: This study investigated ability of NTHi to form biofilms and its impact on airway epithelia using in vivo and in vitro analyses.
Methods: We evaluated bronchoalveolar lavage fluid (BALF) from young CF patients for evidence of NTHi biofilms. To further investigate the pathogenesis of NTHi in respiratory infections, we developed a novel in vitro co-culture model of NTHi biofilm formation on polarized human airway epithelial cells grown at the air-liquid interface.
Measurements and Main Results: In BALF samples from young, asymptomatic CF patients, we found morphologic evidence suggestive of NTHi biofilm formation. Additionally, 10 clinical NTHi isolates from CF patients formed biofilms on plastic surfaces. NTHi formed biofilms on the apical surface of cultured airway epithelia. These biofilms exhibited decreased susceptibility to antibiotics and were adherent to epithelial surfaces. Airway epithelial cells remained viable throughout 4 days of co-culture, and responded to NTHi with NF- Key words: Lung diseases, Bacterial infections, Inflammation
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B signaling, and increased chemokine and cytokine secretion.
Conclusions: NTHi formed adherent biofilms on the apical surface airway epithelia with decreased susceptibility to antibiotics, and respiratory cells exhibited inflammatory and host defense responses-evidence of a dynamic host-pathogen interaction. The data presented here have implications both for understanding early CF lung disease pathogenesis and for the treatment of early, asymptomatic colonization of CF patients with H. influenzae.
