Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Pneumococcal pneumonia is the leading cause of community-acquired pneumonia. Obesity is a risk factor for pneumonia. Host factors play a critical role in susceptibility to pulmonary pathogens and outcome from pulmonary infections. Obesity impairs innate and adaptive immune responses, important in the host defence against pneumococcal disease. One area of emerging interest in understanding the complex relationship between obesity and pulmonary infections is the role of the hormone leptin. There is a substantive evidence base supporting the associations between obesity, leptin, pulmonary infections and host defence mechanisms. Despite this, there is a paucity of research that specifically focuses on Streptococcus pneumoniae (pneumococcal) infections, which are the leading cause of community-acquired pneumonia hospitalisations and mortality worldwide. Much of the evidence examining the role of leptin in relation to S. pneumoniae infections has used genetically mutated mice. The purpose of this mini review is to explore the role leptin plays in the host defence of S. pneumoniae in subjects with obesity and posit an argument for the need for more human research.

Original publication




Journal article


Eur Respir Rev

Publication Date





Animals, Community-Acquired Infections, Humans, Leptin, Lung, Mice, Obesity, Pneumonia, Pneumococcal, Streptococcus pneumoniae