Airway Inflammation in Nonobstructive and Obstructive  Chronic Bronchitis with Chronic <i>Haemophilus influenzae</i>  Airway Infection

Bresser, Paul; Out, Theo A.; Alphen, Loek van; Jansen, Henk M.; Lutter, René

doi:10.1164/ajrccm.162.3.9908103

Cited by 143 publications

(89 citation statements)

References 30 publications

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“…NTHI is the most frequently recovered pathogen from sputum in stable and acutely exacerbated COPD and is associated with more frequent exacerbations and accelerated decline in lung function (4,5,29). The relationship of NTHI with progressive disease in COPD is underscored by an increased risk of exacerbation associated with the acquisition of new respiratory strains of NTHI (2).…”

Section: Discussionmentioning

confidence: 99%

“…Bacterial colonization is associated with advanced airway inflammation, increased frequency of exacerbations, and accelerated decline in lung function, which suggests that bacterial colonization of the lower airways in COPD induces chronic airway inflammation and contributes to progressive airway obstruction (4)(5)(6)(7). Once initiated, chronic inflammation of the lower airways may promote the progression of COPD (3).…”

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confidence: 99%

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Impaired Alveolar Macrophage Response to Haemophilus Antigens in Chronic Obstructive Lung Disease

Berenson

Wrona

Grove

et al. 2006

Am J Respir Crit Care Med

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Rationale: Interactions of nontypeable Haemophilus influenzae (NTHI) with macrophages are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the immunologic mechanisms that mediate NTHI-macrophage inflammation are poorly understood. Outer membrane protein (OMP) P6 and lipooligosaccharide (LOS) of NTHI are potent immunomodulators. We theorized that alveolar macrophages in COPD possess fundamental immune defects that permit NTHI to evade host responses. Objective: To test this hypothesis, we obtained human alveolar and blood macrophages from exsmokers with COPD, exsmokers without COPD, and nonsmokers. Methods: Alveolar and blood macrophages from each donor were incubated with purified LOS and OMP P6 and with OMP P2 and the total outer membrane preparation (0.1-1 g/ml). Measurements: Supernatants (24 h) were assayed for IL-1␤, TNF-␣, IL-10, IL-12, and IL-8 by multianalyte multiplexed flow cytometry. Results: Comparative induction of COPD and non-COPD alveolar macrophages by LOS and OMP P6 revealed diminished IL-8, TNF-␣, and IL-1␤ responses of COPD alveolar macrophages (p р 0.03 for each). COPD alveolar macrophages also had diminished responses to total outer membrane (p р 0.03 for each). In contrast, COPD blood macrophages had no significant differences among donor groups in IL-8, TNF-␣, or IL-1␤ responsiveness to NTHI antigens. Diminished IL-12 responses of COPD blood macrophages to NTHI antigens, compared with nonsmokers, could not be independently dissociated from group differences in age and pack-years. Conclusions: These findings support a paradigm of defective immune responsiveness of alveolar macrophages, but not blood macrophages, in COPD.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Impaired Alveolar Macrophage Response to Haemophilus Antigens in Chronic Obstructive Lung Disease

Berenson

Wrona

Grove

et al. 2006

Am J Respir Crit Care Med

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“…H. influenzae is localised to sites within the airway wall, such as between cells in the airway walls [261] and these organisms are not susceptible to antibiotics or antibody-mediated defence mechanisms when they are located between airway epithelial cells [262]. H. influenzae infection is associated with increased concentrations of inflammatory mediators, including IL-8 and TNF-a, in COPD patients [263]. The inflammatory process itself may also promote persistence of certain bacteria.…”

Section: What Are the Mechanisms Of Acute Exacerbations?mentioning

confidence: 99%

Chronic obstructive pulmonary disease: molecular and cellularmechanisms

Barnes

Shapiro²,

Pauwels³

2003

Eur Respir J

1,228

966

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Chronic obstructive pulmonary disease is a leading cause of death and disability, but has only recently been extensively explored from a cellular and molecular perspective.There is a chronic inflammation that leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterised by increased numbers of alveolar macrophages, neutrophils and cytotoxic T-lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). A high level of oxidative stress may amplify this inflammation. There is also increased elastolysis and evidence for involvement of several elastolytic enzymes, including serine proteases, cathepsins and matrix metalloproteinases.The inflammation and proteolysis in chronic obstructive pulmonary disease is an amplification of the normal inflammatory response to cigarette smoke. This inflammation, in marked contrast to asthma, appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease. Eur Respir J 2003; 22: 672-688.

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“…The presence of bacterial pathogens in the sputum during the stable phase ("bacterial colonization") has been associated with a greater AECOPD frequency (31), poorer health status (32), and a greater decline in lung function (33). Sputum (32,34) and systemic (35) inflammatory markers are elevated in patients with COPD whose sputum is Definition of abbreviations: DGGE = denaturing-gradient gel electrophoresis; TGGE = temperaturegradient gel electrophoresis; T-RFLP = terminal restriction fragment length polymorphisms.…”

Section: Traditional Methods To Establish a Causative Role For Infectmentioning

confidence: 99%

Significance of the Microbiome in Chronic Obstructive Pulmonary Disease

Martínez

Erb-Downward

Huffnagle³

2013

Annals ATS

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Chronic obstructive pulmonary disease (COPD) is one of few chronic disorders with rising mortality and morbidity. It is a highly prevalent disorder, characterized by highly heterogeneous clinical symptoms, health status, and disease progression. COPD is also characterized by an inflammatory/immune response that persists despite smoking cessation and varies by the patient population, method of assessment, and timing of measurement. Bacterial colonization or infection is ubiquitous in patients with COPD and, until recently, has been predominantly assessed using culture-based methodologies. This colonization has been believed to be biologically relevant. It has been estimated that more than 70% of the bacterial species on body surfaces cannot be cultured by standard techniques. As such, advanced culture-independent techniques have been developed that target bacterial genes, such as the 16S ribosomal RNA gene, that function as molecular chronometers. Application of these techniques in patients with COPD has suggested microbial diversity that varies by age, disease severity, and medication use. All of these data provide unique and rapidly evolving insight into the potential role of the respiratory microbiome in disease genesis and expression.

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Airway Inflammation in Nonobstructive and Obstructive Chronic Bronchitis with Chronic Haemophilus influenzae Airway Infection

Cited by 143 publications

References 30 publications

Impaired Alveolar Macrophage Response to Haemophilus Antigens in Chronic Obstructive Lung Disease

Impaired Alveolar Macrophage Response to Haemophilus Antigens in Chronic Obstructive Lung Disease

Chronic obstructive pulmonary disease: molecular and cellularmechanisms

Significance of the Microbiome in Chronic Obstructive Pulmonary Disease

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