Obesity and Respiratory Infections Including COVID-19

Obesity is a well-known risk factor for cardiometabolic disease and is now recognized as an underlying condition linked to immune dysfunction. During the recent COVID-19 and 2009 Influenza A pandemics, obesity was associated with a greater severity of illness due to an ineffective immune response. The mechanisms that underpin immune dysfunction in obesity are often characterized as a low-grade state of chronic inflammation but are complex, particularly during infection. In COVID-19 and influenza virus infections, type I interferon responses are attenuated in the lungs and in peripheral blood leukocytes despite a robust systemic proinflammatory cytokine response. Adipose tissue in obesity produces mediators that enhance blood coagulation and this response is amplified during infection, resulting in the formation of microemboli that compromise gas exchange. Vaccination against viruses produces sufficient antibody titers initially but these titers decline more rapidly in individuals who have overweight or obesity. There is more uncertainty regarding the impact of obesity on community-acquired or nosocomial pneumonias in humans although impairments in pulmonary host defense against bacterial pneumonia have been reported in animal models of obesity. Our understanding of the complex mechanisms by which obesity dysregulates pulmonary innate and adaptive immune responses to infection have increased but more research is needed to translate these findings into more precise clinical interventions.