Airway bacterial colonization: The missing link between COPD and cardiovascular events?

Fuschillo, Salvatore; Martucci, Michele; Donner, Claudio F.; Balzano, Giovanni

doi:10.1016/j.rmed.2012.03.023

Cited by 17 publications

(18 citation statements)

References 99 publications

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“…When systemic inflammation has been measured in patients with PPM detection, the evidence for raised fibrinogen and CRP has been conflicting, and no clear association has been found with bacterial loads [7,12]. However, systemic inflammation, and in particular raised fibrinogen, has been suggested as a possible link between COPD and associated cardiovascular events [23] and also as a potential biomarker to identify patients with a higher risk of mortality [24]. Therefore, the role of fibrinogen in the pathogenesis and clinical outcomes in COPD patients with bacterial colonisation is important area of research for future studies.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory thresholds and the species-specific effects of colonising bacteria in stable chronic obstructive pulmonary disease

et al. 2014

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BackgroundThere has been increasing interest in the use of newer, culture-independent techniques to study the airway microbiome of COPD patients. We investigated the relationships between the three common potentially pathogenic microorganisms (PPMs) Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis, as detected by quantitative PCR (qPCR), and inflammation and health status in stable patients in the London COPD cohort.MethodsWe prospectively collected sputum, serum and plasma samples for analysis of airway bacterial presence and load, and airway and systemic inflammation from 99 stable COPD patients between January 2011 and October 2012. Health status was measured with St George’s Respiratory Questionnaire and COPD Assessment Test.ResultsAirway inflammation and plasma fibrinogen, but not C-reactive protein, were greater in samples with PPM detection (p < 0.001, p = 0.049 and p = 0.261, respectively). Increasing total bacterial load was associated with increasing airway (p < 0.01) but not systemic inflammation (p > 0.05). Samples with high total bacterial loads had significantly higher airway inflammation than both samples without PPM detection and those with lower loads. Haemophilus influenzae presence was associated with significantly higher levels of airway but not systemic inflammation for all given pathogen loads (p < 0.05), and was significantly greater than with other PPMs. No association was observed between inflammation and health status (p > 0.05).ConclusionsAirway and systemic inflammation, as measured by fibrinogen, is greater in stable COPD patients with PPMs detected using the culture-independent qPCR technique. The airway, but not systemic inflammatory response, appears to have a total pathogen-load threshold and appears attributable to Haemophilus influenzae. However, discordance between inflammation and health status was observed.Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-014-0114-1) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Inflammatory thresholds and the species-specific effects of colonising bacteria in stable chronic obstructive pulmonary disease

et al. 2014

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“…There are reports of a subgroup of COPD patients with chronic bacterial airway colonization who are at increased risk for frequent exacerbations, have higher levels of both airway and systemic inflammation, and are at increased risk of cardiovascular complications compared with those without chronic bacterial airway colonization. 43 …”

Section: Copd Phenotypesmentioning

confidence: 99%

Diagnosis, assessment, and phenotyping of COPD: beyond FEV1

Lange

Halpin

O’Donnell

et al. 2016

COPD

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COPD is now widely recognized as a complex heterogeneous syndrome, having both pulmonary and extrapulmonary features. In clinical practice, the diagnosis of COPD is based on the presence of chronic airflow limitation, as assessed by post-bronchodilator spirometry. The severity of the airflow limitation, as measured by percent predicted FEV1, provides important information to the physician to enable optimization of management. However, in order to accurately assess the complexity of COPD, there need to be other measures made beyond FEV1. At present, there is a lack of reliable and simple blood biomarkers to confirm and further assess the diagnosis of COPD. However, it is possible to identify patients who display different phenotypic characteristics of COPD that relate to clinically relevant outcomes. Currently, validated phenotypes of COPD include alpha-1 antitrypsin deficiency, and “frequent exacerbators”. Recently, a definition and assessment of a new phenotype comprising patients with overlapping features of asthma and COPD has been suggested and is known as “asthma COPD overlap syndrome”. Several other phenotypes have been proposed, but require validation against clinical outcomes. Defining phenotypes requires the assessment of multiple factors indicating disease severity, its impact, and its activity. Recognition and validation of COPD phenotypes has an important role to play in the selection of evidence-based targeted therapy in the future management of COPD, but regardless of the diagnostic terms, patients with COPD should be assessed and treated according to their individual treatable characteristics.

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“…It is mainly caused by cigarette smoke and is the fourth leading cause of death worldwide. According to the World Health Organization, its prevalence will double by 2020 [ 1 ] and it will become the third leading cause of death worldwide [ 2 ]. But the mechanism of COPD is not completely illuminated.…”

Section: Introductionmentioning

confidence: 99%

Comparison between cigarette smoke-induced emphysema and cigarette smoke extract-induced emphysema

He¹,

Chen²,

Chen³

et al. 2015

Tob. Induced Dis.

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Background and objectiveEmphysema is the main pathological feature of COPD and also is the focus of the related research. Although several emphysema animal models have been established, exact comparison of findings is seldom. The present study aimed to compare cigarette smoke (CS) exposure-induced emphysema model and intraperitoneal injection of cigarette smoke extract (CSE)-induced emphysema model to evaluate the effectiveness of the two different modeling methods.MethodsSix-week-old male C57BL/6 J mice were used and randomly divided into two groups: CS exposure and intraperitoneal injection of CSE. Each group was subdivided into two subgroups: control and CS or CSE. Lung function, mean linear intercept (MLI), destructive index (DI), apoptotic index (AI), total and differential cells count in broncholavolar lavage fluid (BALF), SOD and IL-6 concentration in serum were measured.ResultsCompared with their respective controls, lung function was significantly decreased in CS and CSE groups (P < 0.01); MLI, DI, and AI of lung tissue were significantly higher in CS and CSE groups (P < 0.01); total number of leukocytes, the number and percentage of neutrophils (NEUs), and the number of macrophages (MAC) in BALF were significantly higher in CS and CSE groups (P < 0.01); SOD concentration in serum was significantly decreased in CS and CSE groups (P < 0.01); IL-6 concentration in serum was significantly increased in in CS and CSE groups (P < 0.01). There was no significant difference between CS group and CSE group in any of the parameters described above.ConclusionsBoth CS exposure and intraperitoneal injection of CSE could induce emphysema and the effectiveness of the two different modeling methods were equal.

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Airway bacterial colonization: The missing link between COPD and cardiovascular events?

Cited by 17 publications

References 99 publications

Inflammatory thresholds and the species-specific effects of colonising bacteria in stable chronic obstructive pulmonary disease

Inflammatory thresholds and the species-specific effects of colonising bacteria in stable chronic obstructive pulmonary disease

Diagnosis, assessment, and phenotyping of COPD: beyond FEV1

Comparison between cigarette smoke-induced emphysema and cigarette smoke extract-induced emphysema

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