Legionella are intracellular bacteria causing Legionnaire´s Disease (LD), a form of pneumonia particularly severe in immunocompromised people. The most common causative species responsible worldwide is L. pneumophila, while in Australia L. longbeachae infections account for up to half of LD cases. Cigarette smoke has been associated with a variety of effects on immune responses in the lung and with increased susceptibility to LD caused by L. pneumophila.
We aim to investigate the immune response towards Legionella infection in mice in the context of acute cigarette smoke exposure to understand how smoking renders individuals more susceptible to infection.
We established and characterized a model of C57BL/6 wild-type mice exposed to cigarette smoke prior to and after infection with Legionella. Smoke exposure particularly affected counts of alveolar macrophages and neutrophils in the lung before and after infection. Initial data showed that L. pneumophila-caused disease progression in mice exposed to cigarette smoke was more severe compared to air exposed mice and bacterial load in the lung was significantly increased. In smoke exposed mice, we also observed that bacteria mainly localized to neutrophils. However, alveolar macrophages were the only cell type that contained elevated levels of viable bacteria. Contrary to that, L. longbeachae infection and concurrent smoke exposure did not intensify disease progression in mice and clearance of bacteria was not impaired.
Our current hypothesis is that alveolar macrophages and neutrophils potentially lose their bactericidal properties and are more permissive for L. pneumophila replication due to smoke exposure. We speculate, that the different phenotypes observed in the infection model using different Legionella species may be related to alveolar macrophage counts in the lung.