Chronic obstructive pulmonary disease is the 3^rd commonest in the world. It is a heterogeneous disease characterised clinically by difficulties in breathing. It is induced by cigarette smoking that causes airway inflammation. Chronic inflammation results in tissue damage leading to airway remodelling and fibrosis, alveolar destruction and emphysema that combine to impair lung function. Current therapies alleviate some symptoms but do not reverse nor cure the disease.  The microbiome encompasses all the microorganisms that inhabit the body. Recent studies show that a healthy microbiome is essential for maintaining homeostasis and health. Alterations in microbiomes in various tissues (eg gut) is associated with disease (eg colitis), potentially by inducing local and systemic inflammation. These changes may be reversed by microbiome transfer (eg colitis). Other recent studies have demonstrated that substantial immune and inflammatory cross-talk occurs between the lung and gut. We investigated the changes that occur in the gut microbiome in a mouse model of COPD that we developed. We used microbiome profiling to identify substantial shifts in microbial populations during the induction and progression of COPD. Transfer of fecal microbiomes from smoking groups to air groups and vice versa was performed, with transfer resulting from coprophagy. This suppressed the development of COPD in smoke-exposed mice exposed to the faeces of non-smoking mice. Profiling identified 2 species associated only with COPD and 2 species associated with protection. Analysis to identify genus-level shifts or key microorganisms that cluster with diseased or healthy states is ongoing.