Huang YJ, Lynch SV. The emerging relationship between the airway microbiota and chronic respiratory disease: clinical implications

Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California San Francisco, 513 Parnassus Avenue, Med Sci S357, San Francisco, CA 94143, USA.
Expert Review of Respiratory Medicine 12/2011; 5(6):809-21. DOI: 10.1586/ers.11.76
Source: PubMed

ABSTRACT Until recently, relationships between evidence of colonization or infection by specific microbial species and the development, persistence or exacerbation of pulmonary disease have informed our opinions of airway microbiology. However, recent applications of culture-independent tools for microbiome profiling have revealed a more diverse microbiota than previously recognized in the airways of patients with chronic pulmonary disease. New evidence indicates that the composition of airway microbiota differs in states of health and disease and with severity of symptoms and that the microbiota, as a collective entity, may contribute to pathophysiologic processes associated with chronic airway disease. Here, we review the evolution of airway microbiology studies of chronic pulmonary disease, focusing on asthma, chronic obstructive pulmonary disease and cystic fibrosis. Building on evidence derived from traditional microbiological approaches and more recent culture-independent microbiome studies, we discuss the implications of recent findings on potential microbial determinants of respiratory health or disease.

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Available from: Susan V Lynch, Aug 30, 2015
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    • "Recent studies have shown that an unhealthy status of the respiratory microbiome persists in high-risk populations, such as infants, the elderly and patients with COPD, CF or bronchiectasis , in whom the microbial communities are much less diversified than those found in healthy individuals [27] [28] [29] [30] [31] [32]. Diversity is a major factor that promotes system stability [33], loss of diversity thus lessens the protective effects of the microbiome and renders patients vulnerable to infection. "
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    ABSTRACT: The human pharyngeal microbiome, which resides at the juncture of digestive and respiratory tracts, may have an active role in the prevention of respiratory tract infections, similar to the actions of the intestinal microbiome against enteric infections. Recent studies have demonstrated that the pharyngeal microbiome comprises an abundance of bacterial species that interact with the local epithelial and immune cells, and together, they form a unique micro-ecological system. Most of the microbial species in microbiomes are obligate symbionts constantly adapting to their unique surroundings. Indigenous commensal species are capable of both maintaining dominance and evoking host immune responses to eliminate invading species. Temporary damage to the pharyngeal microbiome due to the impaired local epithelia is also considered an important predisposing risk factor for infections. Therefore, reinforcement of microbiome homeostasis to prevent invasion of infection-prone species would provide a novel treatment strategy in addition to antibiotic treatment and vaccination. Hence continued research efforts on evaluating probiotic treatment and developing appropriate procedures are necessary to both prevent and treat respiratory infections.
    Genomics Proteomics & Bioinformatics 06/2014; 12(3). DOI:10.1016/j.gpb.2014.06.001
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    • "It has been suggested that the fungal colonization could contribute to or trigger - as do other virus infections (HPV, CMV etc) - pathophysiologic processes associated with lung cancer [19]. However, while there is evidence of the involvement of specific fungal species in asthma, chronic obstructive pulmonary disease (COPD) [20,21] and cystic fibrosis (CF) [21-24], little is known of the airway fungal microbiota in the pathogenesis of lung cancer [19]. "
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    ABSTRACT: Airways of lung cancer patients are often colonized by fungi. Some of these colonizing fungi, under particular conditions, produce cancerogenic mycotoxins. Given the recent interest in the infective origin of lung cancer, with this preliminary study we aim to give our small contribution to this field of research by analysing the fungal microbiome of the exhaled breath condensate of lung cancer patients from Puglia, a region of Italy. We enrolled 43 lung cancer patients and 21 healthy subjects that underwent exhaled breath condensate and bronchial brushing collection. The fungal incidence and nature of sample collected were analysed by using a selected media for Aspergillus species. For the first time we were able to analyse the fungal microbioma of the exhaled breath condensate. 27.9% of lung cancer patients showed a presence of Aspergillus niger, or A. ochraceus or Penicillium ssp. while none of the healthy subjects did so. The results confirmed the high percentage of fungal colonization of the airways of lung cancer patients from Puglia, suggesting the need to conduct further analyses in this field in order to evaluate the exact pathogenetic role of these fungi in lung cancer as well as to propose efficient, empirical therapy.
    BMC Pulmonary Medicine 02/2014; 14(1):22. DOI:10.1186/1471-2466-14-22 · 2.49 Impact Factor
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    • "Using microarray analysis, airway specimens have been analyzed from COPD patients who were being managed for severe respiratory exacerbations [104]. Therefore, a diverse bacterial community is documented to be present during pulmonary exacerbation in the setting of antibiotic administration [105]. Viral infections are detected in 10–15% of sputum sample in stable COPD patients and in 30–60% of patients with COPD exacerbation (62) with rhinoviruses and influenza viruses being most frequently associated with the exacerbations [106]. "
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    ABSTRACT: Increasing evidence indicates that chronic inflammatory and immune responses play key roles in the development and progression of COPD. Recent data provide evidence for a role in the NLRP3 inflammasome in the airway inflammation observed in COPD. Cigarette smoke activates innate immune cells by triggering pattern recognition receptors (PRRs) to release "danger signal". These signals act as ligands to Toll-like receptors (TLRs), triggering the production of cytokines and inducing innate inflammation. In smokers who develop COPD there appears to be a specific pattern of inflammation in the airways and parenchyma as a result of both innate and adaptive immune responses, with the predominance of CD8+ and CD4+ cells, and in the more severe disease, with the presence of lymphoid follicles containing B lymphocytes and T cells. Furthermore, viral and bacterial infections interfere with the chronic inflammation seen in stable COPD and exacerbations via pathogen-associated molecular patterns (PAMPs). Finally, autoimmunity is another novel aspect that may play a critical role in the pathogenesis of COPD. This review is un update of the currently discussed roles of inflammatory and immune responses in the pathogenesis of COPD.
    Mediators of Inflammation 07/2013; 2013:413735. DOI:10.1155/2013/413735 · 3.24 Impact Factor
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