Infections and Airway Inflammation in Chronic Obstructive Pulmonary Disease Severe Exacerbations

Papi, Alberto; Bellettato, Cinzia Maria; Braccioni, Fausto; Romagnoli, Micaela; Casolari, Paolo; Caramori, Gaetano; Fabbri, Leonardo M.; Johnston, Sebastian L.

doi:10.1164/rccm.200506-859oc

Cited by 914 publications

(884 citation statements)

References 42 publications

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“…Other investigators have suggested that up to 60% of exacerbations have been associated with viral infections, including picornaviruses, respiratory syncytial virus (RSV), influenza, and human metapneumoviruses (46)(47)(48)(49)(50)(51). One prospective study of hospitalized patients with AE-COPDs found a viral pathogen in more than 48% of episodes (vs. 6.25% in the stable state), with a similar distribution of viral pathogens as previously noted (52). The most compelling data confirming a role for viruses in the genesis of an AE-COPD come from the experimental model of human rhinovirus (HRV) infection recently published by Mallia and colleagues (53).…”

Section: Virusessupporting

confidence: 60%

“…Bandi and colleagues extended these findings by identifying AE-COPDs caused by H. influenza and noting that an acute viral infection was seen in 45.7% of the events (98). The recent prospective study of Papi and colleagues provides important insight (52). Independent of bacterial versus viral infection, sputum neutrophils were increased in AE-COPD compared with baseline, whereas eosinophilic inflammation was seen in patients with viral or mixed viral/bacterial infection.…”

Section: Bacteriamentioning

confidence: 96%

“…The recent identification of differing inflammatory patterns in the sputum samples of hospitalized patients with an exacerbation suggests a possible additional approach to identify viral versus bacterial etiology; sputum eosinophil values greater than 1.68 3 106/g exhibited a sensitivity of 0.82 and specificity of 0.77 for a viral etiology (52). An extension of this approach has been proposed by the incorporation of sputum inflammatory markers (tumor necrosis factor-a and IL-8) in segregating exacerbations caused by ''common bacteria'' compared with Pseudomonas or nonbacterial etiologies (163).…”

Section: Novel Approachesmentioning

confidence: 99%

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Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Martínez

2007

Proceedings of the American Thoracic Society

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Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the natural history of this chronic lung disorder. These events can be caused by a large number of infectious and noninfectious agents and are associated with an increased local and systemic inflammatory response. Their frequency and severity have been linked to progressive deterioration in lung function and health status. Infectious pathogens ranging from viral to atypical and typical bacteria have been implicated in the majority of episodes. Most therapeutic regimens to date have emphasized broad, nonspecific approaches to bronchoconstriction and pulmonary inflammation. Increasingly, therapy that targets specific etiologic pathogens has been advocated. These include clinical and laboratory-based methods to identify bacterial infections. Further additional investigation has suggested specific pathogens within this broad class. As specific antiviral therapies become available, better diagnostic approaches to identify specific pathogens will be required. Furthermore, prophylactic therapy for at-risk individuals during high-risk times may become a standard therapeutic approach. As such, the future will likely include aggressive diagnostic algorithms based on the combination of clinical syndromes and rapid laboratory modalities to identify specific causative bacteria or viruses.

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Section: Virusessupporting

confidence: 60%

Section: Bacteriamentioning

confidence: 96%

Section: Novel Approachesmentioning

confidence: 99%

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Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Martínez

2007

Proceedings of the American Thoracic Society

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“…It's also a feature common to all stages of chronic obstructive pulmonary disease (4) and increased neutrophil levels are reported in induced sputum of chronic obstructive pulmonary disease patients during exacerbations (5).…”

mentioning

confidence: 99%

Myeloperoxidase Deficiency Attenuates Lipopolysaccharide-Induced Acute Lung Inflammation and Subsequent Cytokine and Chemokine Production

Haegens

Heeringa

Suylen

et al. 2009

The Journal of Immunology

103

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Lung neutrophilia is common to a variety of lung diseases. The production of reactive oxygen and nitrogen species during neutrophil oxidative burst has been associated with protein and DNA damage. Myeloperoxidase (MPO) is an enzyme stored in the azurophilic granula of neutrophils. It is important in host defense because it generates the reactive oxidant hypochlorous acid and has been described to play a role in the activation of neutrophils during extravasation. We hypothesized that MPO contributes directly to the development of acute lung neutrophilia via stimulation of neutrophil extravasation and indirectly to the subsequent production of cytokines and chemokines in the lung. To test this hypothesis, wild-type (WT) and Mpo−/− mice were given a single LPS instillation, after which the development of neutrophil-dominated lung inflammation, oxidative stress, and cytokine and chemokine levels were examined. Mpo−/− mice demonstrated a decreased lung neutrophilia that peaked earlier than neutrophilia in WT mice, which can be explained by decreased neutrophil chemoattractant levels in LPS-exposed Mpo−/− compared with WT mice. However, oxidative stress levels were not different in LPS-exposed WT and Mpo−/− mice. Furthermore, in vivo findings were confirmed by in vitro studies, using isolated neutrophils. These results indicate that MPO promotes the development of lung neutrophilia and indirectly influences subsequent chemokine and cytokine production by other cell types in the lung.

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“…La mayoría de los estudios de etiología y evaluación de los marcadores de inflamación sistémi-ca han sido realizados en pacientes hospitalizados por exacerbaciones graves de la EPOC [21][22][23][24][25][26] . Sin embargo, gran parte de las exacerbaciones son manejadas en el ámbito ambulatorio debido a su bajo riesgo de complicaciones y muerte 1,2 .…”

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Etiología y biomarcadores de inflamación sistémica en las exacerbaciones leves a moderadas de la enfermedad pulmonar obstructiva crónica

et al. 2012

Rev. méd. Chile

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Infections and Airway Inflammation in Chronic Obstructive Pulmonary Disease Severe Exacerbations

Cited by 914 publications

References 42 publications

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Myeloperoxidase Deficiency Attenuates Lipopolysaccharide-Induced Acute Lung Inflammation and Subsequent Cytokine and Chemokine Production

Etiología y biomarcadores de inflamación sistémica en las exacerbaciones leves a moderadas de la enfermedad pulmonar obstructiva crónica

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