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Macrolides, inflammation and the lung microbiome: untangling the web of causality
  1. Robert P Dickson1,
  2. Alison Morris2,3
  1. 1Division of Pulmonary and Critical Care Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA
  2. 2Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
  3. 3Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
  1. Correspondence to Professor Robert P Dickson, Division of Pulmonary and Critical Care Medicine, University of Michigan Health System, 6220 MSRB III/SPC 5642, 1150 W. Medical Center Dr., Ann Arbor, MI 48109-5642, USA; rodickso{at}med.umich.edu

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In the past decade, our understanding of the microbiology of the respiratory tract has been revolutionised by the introduction of culture-independent techniques of microbial identification.1 The lungs, once considered sterile in the absence of infection, have been consistently shown to contain diverse microbial communities, even in health.2 One consistent observation in the field is that in virtually every comparison to date, lung microbiota of healthy subjects differ from the lung microbiota of patients with acute and chronic lung disease. Yet, the field faces a crucial and challenging question: Are bacterial communities in the lung altered because of respiratory disease, or are our patients' lungs diseased because of their altered bacterial communities?

Sorting out cause and effect here is an intimidating task: the microbiome and the host response are so tightly entwined that trying to isolate the effects of each is difficult, both practically and conceptually. Most studies to date in the nascent lung microbiome field have been retrospective and descriptive, replete with provocative correlations, but silent on the direction of causality. Few longitudinal studies have provided the means of determining temporally whether dysbiosis arises before lung disease or vice versa. Given the long chronicity and unpredictability of many lung diseases, prospective cohort studies would need to be impractically large and lengthy to determine temporal precedence. Though animal models hold promise to help unravel mechanisms of pathogenesis3 ,4 characterising the lung microbiota of small animals is technically challenging, and the relevance of animal-associated microbiota to human respiratory health is far from obvious. Some innovative recent studies have attempted ‘lung microbiome transplants’ between diseased and non-diseased animals4 ,5 though it has not been established how much of the effect of this exposure is attributable to transferred microbiota and …

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