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Published ahead of print on April 1, 2005, doi:10.1164/rccm.200412-1687OC

Am. J. Respir. Crit. Care Med., Volume 172, Number 1, July 2005, 85-91

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Submitted on December 15, 2004
Accepted on March 30, 2005

Haemophilus influenzae from COPD Patients with Exacerbation Induce More Inflammation than Colonizers

Cecilia L Chin1, Lori J Manzel1, Erin E Lehman1, Alicia L Humlicek1, Lei Shi1, Timothy D Starner2, Gerene M Denning1, Timothy F Murphy3, Sanjay Sethi3, and Dwight C Look1*

1 Department of Internal Medicine, University of Iowa Carver College of Medicine, and Veterans Administration Medical Center, Iowa City, Iowa, USA, 2 Department of Pediatrics, University of Iowa Carver College of Medicine, and Veterans Administration Medical Center, Iowa City, Iowa, USA, 3 Department of Medicine, State University of New York at Buffalo, Buffalo, New York, USA

* To whom correspondence should be addressed. E-mail: dwight-look{at}uiowa.edu.

Rationale: Airway infection with Haemophilus influenzae causes airway inflammation and isolation of new strains of this bacteria is associated with increased risk of exacerbations in patients with chronic obstructive pulmonary disease (COPD). Objective: To determine whether strains of H. influenzae associated with exacerbations cause more inflammation than strains that colonize the airways of COPD patients. Methods: Exacerbation strains of H. influenzae were isolated from patients during exacerbation of clinical symptoms with subsequent development of a homologous serum antibody response, and were compared to colonization strains that were not associated with symptom worsening or an antibody response. Bacterial strains were compared using an in vivo mouse model of airway infection and in vitro cell culture model of bacterial adherence and defense gene and signaling pathway activation in primary human airway epithelial cells. Results: H. influenzae associated with exacerbations caused more airway neutrophil recruitment compared to colonization strains in the mouse model of airway bacterial infection. Furthermore, exacerbation strains adhered to epithelial cells in significantly higher numbers and induced more interleukin-8 release after interaction with airway epithelial cells. This effect was likely mediated by increased activation of the nuclear factor-{kappa}B and p38 mitogen-activated protein kinase signaling pathways. Conclusions: The results indicate that H. influenzae strains isolated from patients during COPD exacerbations often induce more airway inflammation and likely have differences in virulence compared to colonizing strains. These findings support the concept that bacteria infecting the airway during COPD exacerbations mediate increased airway inflammation and contribute to decreased airway function.
Key words: Neutrophil infiltration, Bacterial adhesion, Interleukin-8, NF-kappaB, p38 mitogen-activated protein kinases




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