Current Concepts: Infection in the Pathogenesis and Course of Chronic Obstructive Pulmonary Disease

Division of Pulmonary and Critical Medicine, Department of Medicine, University at Buffalo, State University of New York, and Department of Veterans Affairs Western New York Healthcare System, Buffalo 14215, USA.
New England Journal of Medicine (Impact Factor: 54.42). 12/2008; 359(22):2355-65. DOI: 10.1056/NEJMra0800353
Source: PubMed
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    • "" Inflamm-aging " often takes place and is associated with immunosuppression and low grade inflammation [69]. When secondary pulmonary infection occurs as a result of impaired host response, secondary inflammation develops [73]. "
    Mediators of Inflammation 06/2015; 2015(692546):1. · 3.24 Impact Factor
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    • "Therefore, a novel systemic biomarker with genetic and mechanistic correlations to the etiology of COPD and/or its exacerbation is needed (Carter et al. 2011, 2013). Most cases of COPD exacerbation are thought to be triggered by airway infection (Sethi and Murphy 2008). In a previous genotype–phenotype correlation study, we found that COPD patients without Siglec-14 were less prone to exacerbation (Angata et al. 2013). "
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    ABSTRACT: We have previously demonstrated that chronic obstructive pulmonary disease (COPD) patients who do not have Siglec-14 are less prone to exacerbation of the disease. Siglec-14 is a myeloid cell protein that recognizes bacteria and triggers inflammatory responses. Therefore, soluble mediators secreted by myeloid cells responding to Siglec-14 engagement could be involved in the pathogenesis of exacerbation and could potentially be utilized as biomarkers of exacerbation. To find out, we sought genes specifically induced in Siglec-14+ myeloid cells and evaluated their utility as biomarkers of COPD exacerbation. Using DNA microarray, we compared gene expression levels in Siglec-14+ and control myeloid cell lines stimulated with or without nontypeable Haemophilus influenzae to select genes that were specifically induced in Siglec-14+ cells. The expressions of several cytokine and chemokine genes were specifically induced in Siglec-14+ cells. The concentrations of seven gene products were analyzed by multiplex bead array assays in paired COPD patient sera (n = 39) collected during exacerbation and stable disease states. Those gene products that increased during exacerbation were further tested using an independent set (n = 32) of paired patient sera. Serum concentration of interleukin-27 (IL-27) was elevated during exacerbation (discovery set: P = 0.0472; verification set: P = 0.0428; combined: P = 0.0104; one-sided Wilcoxon matched-pairs signed-rank test), particularly in exacerbations accompanied with sputum purulence and in exacerbations lasting more than a week. We concluded that IL-27 might be mechanistically involved in the exacerbation of COPD and could potentially serve as a systemic biomarker of exacerbation.
    07/2014; 2(7). DOI:10.14814/phy2.12069
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    • "Although the associations between lower respiratory tract infection during the major period of postnatal growth and impaired lung function in adulthood are now well established, there is ongoing debate whether this association reflects a cause–effect relationship. An alternative explanation for the observed association is that an impaired lung growth antedates the respiratory tract infection, with the infectious episode as a result of the vulnerability of smaller lungs to infection [57]. Further studies are warranted to investigate whether protracted bacterial bronchitis is a risk factor for developing COPD. "
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    ABSTRACT: Cough may be the first overt sign of disease of the airways or lungs when it represents more than a defense mechanism, and may by its persistence become a helpful pointer of potential disease for both patient and physician. On the other hand, impairment or absence of the coughing mechanism can be harmful and even fatal; this is why cough suppression is rarely indicated in childhood. Pediatricians are concerned more with the etiology of the cough and making the right diagnosis. Whereas chronic cough in adults has been universally defined as a cough that lasts more than 8weeks, in childhood, different timing has been reported. Many reasons support defining a cough that lasts more than 4weeks in preschool children as chronic, however; and this is particularly true when the cough is wet. During childhood, the respiratory tract and nervous system undergo a series of anatomical and physiological maturation processes that influence the cough reflex. In addition, immunological response undergoes developmental and memorial processes that make infection and congenital abnormalities the overwhelming causes of cough in preschool children. Cough in children should be treated on the basis of etiology, and there is no evidence in support of the use of medication for symptomatic cough relief or adopting empirical approaches. Most cases of chronic cough in preschool age are caused by protracted bacterial bronchitis, tracheobronchomalacia, foreign body aspiration, post-infectious cough or some combination of these. Other causes of chronic cough, such as bronchiectasis, asthma, gastroesophageal reflux, and upper respiratory syndrome appear to be less frequent in this age group. The prevalence of each depends on the population in consideration, the epidemiology of infectious diseases, socioeconomic aspects, and the local health system.
    Early human development 09/2013; DOI:10.1016/j.earlhumdev.2013.07.018 · 1.93 Impact Factor
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