Obesity-Mediated Alterations in Immune Function, Host Defense, and Lung Disease

Obesity is one of the foremost chronic conditions affecting humans globally and is associated with myriad diseases affecting most organs, including the lungs. One of the underlying mechanisms is its effect on innate and adaptive immune systems. Macrophages are the sentinel cell type associated with adipose tissue inflammation and play a key role in obesity-mediated lung diseases. They are activated in the setting of hypoxia, as occurs in obstructive sleep apnea (OSA). They are less effective at clearing viral and bacterial infections and have decreased efferocytosis. Among adaptive responses, T helper 1 cells with pro-inflammatory nonallergic patterns have been associated with OSA and obesity-related asthma. Less is known about B cell function in obesity. In obese asthma, neutrophilic airway inflammation has been better defined in adults as compared to children; there is also evidence to suggest a role of eosinophilic as well as paucigranulocytic airway inflammation. Although substantial inroads have been made in understanding the contribution of obesity-mediated immune dysregulation to pulmonary diseases, areas for further investigations include innate cells other than macrophages, and B cells and eosinophils. There is also need for investigation of the interactions between innate and adaptive immune responses.