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


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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    • "Recent studies show that the lower respiratory tract is a microbial reservoir in HIV-infected individuals rather than being a sterile environment as observed in healthy non-infected subjects and this may contribute to recurrent pneumonia and COPD in HIV-infected patients (Huang et al., 2011; Iwai et al., 2012). Moreover, the lung microbiome in People living with HIV is similar to that observed in COPD and cystic fibrosis (Huang and Lynch, 2011). Impaired MCC, is primarily responsible for microbial colonization of airways in chronic airway diseases like COPD and cystic fibrosis (Sethi, 2000; Livraghi and Randell, 2007). "
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    ABSTRACT: Impaired mucociliary clearance (MCC) is a hallmark of acquired chronic airway diseases like chronic bronchitis associated with chronic obstructive pulmonary disease (COPD) and asthma. This manifests as microbial colonization of the lung consequently leading to recurrent respiratory infections. People living with HIV demonstrate increased incidence of these chronic airway diseases. Bacterial pneumonia continues to be an important comorbidity in people living with HIV even though anti-retroviral therapy has succeeded in restoring CD4+ cell counts. People living with HIV demonstrate increased microbial colonization of the lower airways. The microbial flora is similar to that observed in diseases like cystic fibrosis and COPD suggesting that mucociliary dysfunction could be a contributing factor to the increased incidence of chronic airway diseases in people living with HIV. The three principal components of the MCC apparatus are, a mucus layer, ciliary beating, and a periciliary airway surface liquid (ASL) layer that facilitates ciliary beating. Cystic fibrosis transmembrane conductance regulator (CFTR) plays a pivotal role in regulating the periciliary ASL. HIV proteins can suppress all the components of the MCC apparatus by increasing mucus secretion and suppressing CFTR function. This can decrease ASL height leading to suppressed ciliary beating. The effects of HIV on MCC are exacerbated when combined with other aggravating factors like smoking or inhaled substance abuse, which by themselves can suppress one or more components of the MCC system. This review discusses the pathophysiological mechanisms that lead to MCC suppression in people living with HIV who also smoke tobacco or abuse illicit drugs.
    Frontiers in Microbiology 11/2015; 6:1052. DOI:10.3389/fmicb.2015.01052 · 3.99 Impact Factor
    • "As pioneers, Laurenzi et al. (1961), Pecora (1963), Austrian (1968) and also Murray et al. (2013), based on traditional culture-based methods, have revealed that ''the lungs are sterile organs'' (Austrian, 1968; Laurenzi et al., 1961; Murray et al., 2013; Pecora, 1963). On the other hand, other studies by Monso et al. (1999), Harris et al. (2007), Bousbia et al. (2010), Hilty et al. (2010), Charlson et al. (2011), Erb-Downward et al. (2011) and Huang et al. (2011), Sze et al. (2012), Duff et al. (2013), Garzoni et al. (2013), Rogers et al. (2013) and Segal et al. (2013) and Sze et al. (2014) supported the contradictory concept that lungs are not sterile using culture-independent methods based on genomics and metagenomics (Bousbia et al., 2010; Charlson et al., 2011; Duff et al., 2013; Erb-Downward et al., 2011; Garzoni et al., 2013; Harris et al., 2007; Hilty et al., 2010, Huang et al., 2011; Monso et al., 1999; Rogers et al., 2013; Segal et al., 2013; Sze et al., 2012, 2014). Thus, as listed in Table 1, different studies have resulted in distinct outcomes for and against the presence of lung microbiome. "
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    ABSTRACT: The concept of microbial content of the lung is still controversial. What make this more complicated are controversial results obtaining from different methodologies about lung microbiome and the definition of ‘‘lung sterility’’. Lungs may have very low bacteria but are not completely germ-free. Bacteria are constantly entering from the upper respiratory tract, but are then quickly being cleared. We can find bacterial DNA in the lungs, but it is much harder to ask about living bacteria. Here, we propose that if there is any trafficking of the microorganisms in the lung, it should be a ‘‘Transient But Not Resident (TBNR)’’ model. So, we speculate a "Yin Yang model" for the lung immune system and TBNR. Despite beneficial roles of microbiome on the development of lung immune system, any disruption and alteration in the microbiota composition of upper and lower airways may trigger or lead to several diseases such as asthma, chronic obstructive pulmonary disease and mustard lung disease.
    Inhalation Toxicology 08/2015; DOI:10.3109/08958378.2015.1070220 · 2.26 Impact Factor
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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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