Thus, low urinary bile acid excretion in obese type 2 diabetic patients may reflect cytokine suppression, which in turn may have damaging effects on glucose homeostasis. In support of this, post-prandial plasma bile acid response is blunted in the obese, and several bile acid metabolites are associated with insulin sensitivity. Chemically reducing bile acid pool size in animal models induces both diabetes mellitus and obesity, supporting the hypothesis that the suppressed urinary bile acid output seen in the obese in this study is of pathological significance. One of the limitations of the study is the small cohort. The small numbers were the consequence of the strict selection criteria applied to try to avoid any influence of confounding factors on bile acid metabolism. Despite this, study numbers were sufficient to demonstrate the profound glycaemia-related changes in bile acid metabolism in normal weight and overweight type 2 diabetes. The data in this study argue that at least for the obese type 2 diabetes patients, restoration of bile acid metabolism may be beneficial. Weight loss is associated with improvements in bile acid metabolism. Bariatric surgery provides the most significant and durable weight loss, but remission of type 2 diabetes mellitus precedes significant weight loss. This may be associated with enhanced b-cell function, hepatic insulin sensitivity, and nutrient rerouting, which many studies have causally related to the improved post-prandial GLP-1 responses. , and may thus contribute to type 2 diabetes remission perhaps via GLP-1. Weight loss by dietary means alone has also been shown to improve post-prandial GLP-1 response in the obese although bile acids were not measured. In summary, the data in this study show that bile acids are increased in type 2 diabetes mellitus as a function of glycaemia in individuals with a BMI below 30 kg/m2. This is consistent with glucose stimulating bile acid production to maintain glucose homeostasis, possibly by increased GLP-1 response and altering FXR mediated signalling. Understanding how these compensatory mechanisms are lost in obese individuals with type 2 diabetes may provide an avenue for the development of new therapeutic strategies. Epithelial cells are the most studied cells involved in release of HRV-induced cytokines; however, a number of studies indicate that the macrophage is also important in HRV pathogenesis. Because macrophages are the second-largest cell population in the lungs and the largest population of immune cells, they may play an important role in the inflammatory response resulting from HRV infection. Several reports have demonstrated that peripheral blood monocyte-derived macrophages and alveolar macrophages behave identically to HRV exposure in signaling and cytokine secretion. This observation, coupled with both the comparative ease in harvesting MDMs and the lack of viral replication, makes this an idea cell type in which to examine.