Complex interface between immunity and metabolism: The lung as a target organ

For decades, overweight and obesity have been considered the result of the complex intersection between genes and environment, and their pathogenesis is still unknown. Obesity is associated with insulin resistance and dyslipidaemia, and accumulating evidence indicates that a state of chronic inflammation has a crucial role in the pathogenesis of obesity-related metabolic dysfunction. Excess adipose mass leads to increased levels of proinflammatory cytokines, and interventions aimed at inducing weight loss lead to an overall improvement of the inflammatory state. In this context, the discovery of the adipose tissue-derived hormone, leptin, and other adipocytokines has shed fundamental insights on the basic mechanisms governing immune tolerance in the context of metabolic disease susceptibility. Here, we review how overweight, obesity, and metabolic dysregulation affect lung physiology and pathophysiology in a context of rapidly expanding experimental and clinical data that support the potential role for immunometabolism in the pathogenesis of lung diseases and their complications.