Do Bacteria Cause Exacerbations of COPD?

Hirschmann, Jan V.

doi:10.1378/chest.118.1.193

Cited by 108 publications

(72 citation statements)

References 71 publications

(91 reference statements)

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“…It is known that some microorganisms, including S. pneumoniae, can colonize the airways of COPD patients in a stable state (9). This colonization has been associated with an increase in frequency of symptom exacerbations (7), which are linked with a reduction in quality of life (22,23) and increased health care costs (1).…”

Section: Discussionmentioning

confidence: 99%

“…As well as this association with an increase in exacerbation frequency, colonizing bacteria are also considered a comorbid condition that contributes to the pathogenesis and clinical course of COPD, independently of exacerbations (8). The three most common bacterial species to colonize the lungs in stable-state COPD are nontypeable Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis (9). Current in vivo models of infection with these pathogens are acute and do not mimic the low-level-persistent bacterial presence seen inwere confirmed by optochin sensitivity, Gram stain, catalase reaction, and ␣-hemolysis on blood agar plates.…”

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Development and Characterization of a Long-Term Murine Model of Streptococcus pneumoniae Infection of the Lower Airways

et al. 2014

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cChronic obstructive pulmonary disease (COPD) is characterized by long periods of stable symptoms, but exacerbations occur, which result in a permanent worsening of symptoms. Previous studies have shown a link between bacterial colonization of the lower airways of COPD sufferers and an increase in exacerbation frequency. One of the most frequent bacterial colonizers is Streptococcus pneumoniae. To mimic this aspect of COPD, a murine model of low-level pneumococcal colonization in the lung has been developed, in which S. pneumoniae persisted in the lungs for at least 28 days. From day 14 postinfection, bacterial numbers remained constant until at least 28 days postinfection, and animals showed no outward signs of disease. The bacterial presence correlated with a low-level inflammatory response that was localized to small foci across the left and inferior lobes of the lung. The cellular response was predominantly monocytic, and focal fibroplasia was observed at the airway transitional zones. Physiological changes in the lungs were investigated with a Forced Maneuvers system. This new model provides a means of study of a long-term pulmonary infection with a human pathogen in a rodent system. This is an excellent tool for the development of future models that mimic complex respiratory diseases such as COPD and asthma.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Development and Characterization of a Long-Term Murine Model of Streptococcus pneumoniae Infection of the Lower Airways

et al. 2014

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“…While the primary cause of COPD is smoking or exposure to other inhaled pollutants, the progression and severity of COPD may be promoted by opportunistic airway infections (37). While this has been an area of some controversy (9), it is undeniable that the management of COPD is, at best, seriously complicated by bacterial and viral infections (31). The agents that cause COPD-related airway infections are found predominantly within the normal flora of the nasopharynx and include nontypeable Haemophilus influenzae (NTHi), Streptococcus pneumoniae, Moraxella catarrhalis, and Pseudomonas aeruginosa (25,26,37,38).…”

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Diminished ICAM-1 Expression and Impaired Pulmonary Clearance of NontypeableHaemophilus influenzaein a Mouse Model of Chronic Obstructive Pulmonary Disease/Emphysema

Pang¹,

Hong²,

West-Barnette³

et al. 2008

Infect Immun

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The airways of patients with chronic obstructive pulmonary disease (COPD) are continually colonized with bacterial opportunists like nontypeable Haemophilus influenzae (NTHi), and a wealth of evidence indicates that changes in bacterial populations within the lung can influence the severity of COPD. In this study, we used a murine model for COPD/emphysema to test the hypothesis that COPD affects pulmonary clearance. Mice were treated with a pulmonary bolus of elastase, and as reported previously, the lungs of these mice were pathologically similar to those with COPD/emphysema at ϳ1 month posttreatment. Pulmonary clearance of NTHi was significantly impaired in elastase-treated versus mock-treated mice. While histopathologic analysis revealed minimal differences in localized lung inflammation between the two groups, lower levels of intercellular adhesion molecule 1 (ICAM-1) were observed for the airway epithelial surface of elastase-treated mice than for those of control mice. Following infection, elastase-treated mice had lung pathology consistent with pneumonia for as long as 72 h postinfection, whereas at the same time point, mock-treated mice had cleared NTHi and showed little apparent pathology. Large aggregates of bacteria were observed within damaged lung tissue of the elastase-treated mice, whereas sparse individual bacteria were observed in lungs of mock-treated mice at the same time point postinfection. Additional infection studies showed that NTHi mutants with biofilm defects were less persistent in the elastase-treated mice than the parent strain. These findings establish a model for COPD-related infections and support the hypotheses that ICAM-1 promotes clearance of NTHi. Furthermore, the data indicate that NTHi may form biofilms within the context of COPD-related infections.

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“…For many years, there has been controversy regarding whether bacteria play a role in AECOPD, and thus, whether antibiotics play a role in disease management [3,4]. Several studies have shown an association between the presence of certain bacterial species, such as Streptococcus pneumoniae, Moraxella catarrhalis and Haemophilus influenzae, and AECOPD [3].…”

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The role of atypical respiratory pathogens in exacerbations of chronic obstructive pulmonary disease

Diederen¹,

Valk²,

Kluytmans³

et al. 2007

Eur Respir J

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The aetiology of acute exacerbations of chronic obstructive pulmonary disease (COPD) is heterogeneous and still under discussion. Serological studies have suggested that Mycoplasma pneumoniae, Chlamydia pneumoniae and Legionella pneumophila may play a role in acute exacerbations of COPD.The presence of these atypical pathogens in sputum samples was investigated in patients with stable COPD and with acute exacerbations of COPD using real-time PCR. The present study was part of a randomised, double-blind, single-centre study and a total of 248 sputum samples from 104 COPD patients were included. In total, 122 samples obtained during stable disease (stablestate sputa) and 126 samples obtained during acute exacerbations of COPD (exacerbation sputa) were tested.Of the 122 stable-state sputa, all samples were negative for M. pneumoniae and C. pneumoniae DNA, whereas one sample was positive for Legionella non-pneumophila DNA. Of the 126 exacerbation sputa, all samples were negative for M. pneumoniae and C. pneumoniae DNA, whereas one sample was positive for Legionella non-pneumophila DNA.The possible relationship between the presence of atypical pathogens and the aetiology of acute exacerbations in chronic obstructive pulmonary disease was investigated in patients with stable disease and in those with acute exacerbations using real-time PCR. No indication was found of a role for Legionella spp., Chlamydia pneumoniae or Mycoplasma pneumoniae in stable, moderately severe chronic obstructive pulmonary disease and in its exacerbations.

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Do Bacteria Cause Exacerbations of COPD?

Cited by 108 publications

References 71 publications

Development and Characterization of a Long-Term Murine Model of Streptococcus pneumoniae Infection of the Lower Airways

Development and Characterization of a Long-Term Murine Model of Streptococcus pneumoniae Infection of the Lower Airways

Diminished ICAM-1 Expression and Impaired Pulmonary Clearance of NontypeableHaemophilus influenzaein a Mouse Model of Chronic Obstructive Pulmonary Disease/Emphysema

The role of atypical respiratory pathogens in exacerbations of chronic obstructive pulmonary disease

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