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The Role of Haemophilus parainfluenzae in COPD^*

^* From the Department of Respiratory Medicine (Drs. Hill, Mitchell, and Stockey), Queen Elizabeth Hospital, Birmingham; and Host Defence Unit (Dr. Wilson), Royal Brompton Hospital, London, UK.

Correspondence to: Susan L. Hill, PhD, Lung Investigation Unit, 1st Floor Nuffield House, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2th, UK

	Introduction

TOP Introduction

 
Abbreviations: HPI = Haemophilus parainfluenzae; NTHI = nontypeable Haemophilus influenzae; OMP = outer membrane protein

The role of Haemophilus parainfluenzae (HPI) in COPD infection is unclear, in contrast to the accepted pathogenicity of its close relative nontypeable Haemophilus influenzae (NTHI). We have examined the incidence of HPI in patients with COPD and assessed its interaction with host defense systems and with respiratory epithelium.

We recovered HPI in mean viable numbers of 5.8 x 10⁷ cfu/mL (range, 1 x 10⁵ to 1.5 x 10⁹) in 25% of stable patients under hospital care with moderate to severe COPD, and in 18% of 138 patients studied in the community at the start of an acute exacerbation of COPD. Characterization of pathogenic factors revealed that 11% of 72 HPI strains were haemolytic and produced IgA₁ protease, an enzyme potentially important in colonization of mucosal surfaces. ß-Lactamase production was demonstrated in 28% of HPI isolates and, in general, reduced susceptibility to many commonly prescribed antibiotic agents was observed. HPI-specific serum IgG was increased (p < 0.01) in COPD patients where HPI had been recovered compared to normal healthy control subjects. Marked interstrain variation, suggesting the potential for immune evasion, was seen in outer membrane protein (OMP) profiles of 46 isolates obtained from 27 patients. Western blotting confirmed serum and sputum antibody recognition of 16, 36, and 22 KD OMPs of HPI that were shown by absorption and elution experiments to possess epitopes exposed on the surface of the intact bacterium. Two strains of HPI adhered poorly to the respiratory mucosa, but still caused extensive epithelial cell damage and slowed ciliary beat frequency in organ culture and nasal epithelium models of infection. In addition, these strains stimulated production of the potent neutrophil chemoattractant, interleukin-8 by cultured respiratory epithelial cells (A549s) in a similar way to NTHI.

These studies indicate that further investigation of the role of HPI in COPD is warranted, since it has the potential to play a role in the pathogenesis of COPD infection in a similar way to that observed for NTHI.

This Article Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hill, S. L. Articles by Wilson, R. Search for Related Content PubMed PubMed Citation Articles by Hill, S. L. Articles by Wilson, R.