To model the common clinical scenario of sepsis followed by pneumonia, researchers systemically treated models with a bacterial product that would elicit a sepsis-like response, followed hours later by a live bacterial challenge in the lungs. One group of models had completely normal livers, and the other lacked a gene in their livers that prevented maximal liver activation.
The study showed those in the group lacking a complete liver response exhibited a significantly compromised immune response in both the lungs and blood, where more bacteria survived, and were ultimately more likely to succumb to pneumonia.
According to corresponding author Lee J. Quinton, PhD, associate professor of medicine and pathology at BUSM, “The results of this study directly suggest that liver activation is required to maintain adequate immune responses in the lungs.”
The authors suggest that liver activity may serve as a previously unrealized window into pneumonia defense and susceptibility.
“A better understanding of how these distinct organs collaborate to mount immune responses has important clinical implications for patients with or at risk for pneumonia and sepsis,” said Dr. Quinton. “The idea that non-lung tissue could be targeted for treatments of lung disease is compelling.”
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