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Impaired alveolar macrophage response to Haemophilus antigens in chronic obstructive lung disease

Charles S Berenson1, Catherine T Wrona, Lori J Grove

  • 1Infectious Disease Division, Department of Veterans Affairs Western New York Healthcare System, State University of New York at Buffalo School of Medicine, Buffalo, NY 14215, USA. berenson@acsu.buffalo.edu

American Journal of Respiratory and Critical Care Medicine
|April 1, 2006
PubMed
Abstract

Insights

Alveolar macrophages in chronic obstructive pulmonary disease (COPD) show immune defects, leading to reduced responses to nontypeable Haemophilus influenzae (NTHI) antigens. Blood macrophages in COPD patients do not exhibit these same immune deficiencies.

Area of Science:

  • Immunology
  • Pulmonology
  • Microbiology

Background:

  • Nontypeable Haemophilus influenzae (NTHI) interactions with macrophages are crucial in chronic obstructive pulmonary disease (COPD) pathogenesis.
  • The specific immune mechanisms underlying NTHI-macrophage inflammation in COPD remain unclear.
  • Outer membrane protein (OMP) P6 and lipooligosaccharide (LOS) from NTHI are known potent immunomodulators.

Purpose of the Study:

  • To investigate potential immune defects in alveolar macrophages from COPD patients.
  • To compare the immune responses of alveolar and blood macrophages from COPD patients, healthy ex-smokers, and non-smokers when exposed to NTHI components.
  • To determine if COPD-associated immune dysfunction is specific to alveolar macrophages.

Main Methods:

  • Human alveolar and blood macrophages were isolated from three groups: ex-smokers with COPD, ex-smokers without COPD, and non-smokers.
  • Macrophages were incubated with purified NTHI antigens: lipooligosaccharide (LOS), outer membrane protein (OMP) P6, OMP P2, and total outer membrane preparations.
  • Cytokine levels (IL-1beta, TNF-alpha, IL-10, IL-12, IL-8) in culture supernatants were measured using multiplexed flow cytometry after 24 hours.

Main Results:

  • COPD alveolar macrophages exhibited significantly diminished IL-8, TNF-alpha, and IL-1beta responses to LOS and OMP P6 compared to non-COPD alveolar macrophages.
  • Responses of COPD alveolar macrophages to total NTHI outer membrane preparation were also significantly reduced.
  • In contrast, COPD blood macrophages showed no significant differences in IL-8, TNF-alpha, or IL-1beta responsiveness to NTHI antigens compared to other groups.

Conclusions:

  • Alveolar macrophages in individuals with COPD display fundamental immune defects.
  • These defects result in impaired inflammatory responses to key NTHI components.
  • Immune dysfunction observed in COPD appears specific to alveolar macrophages, as blood macrophages do not show similar deficiencies.

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