Abstract
Chlamydiae are intracellular bacteria that commonly cause infections of the respiratory and genital tracts, which are major clinical problems. Infections are also linked to the aetiology of diseases such as asthma, emphysema and heart disease. The clinical management of infection is problematic and antibiotic resistance is emerging. Increased understanding of immune processes that are involved in both clearance and immunopathology of chlamydial infection is critical for the development of improved treatment strategies. Here, we show that IL-13 was produced in the lungs of mice rapidly after Chlamydia muridarum (Cmu) infection and promoted susceptibility to infection. Wild-type (WT) mice had increased disease severity, bacterial load and associated inflammation compared to IL-13 deficient (−/−) mice as early as 3 days post infection (p.i.). Intratracheal instillation of IL-13 enhanced bacterial load in IL-13−/− mice. There were no differences in early IFN-g and IL-10 expression between WT and IL-13−/− mice and depletion of CD4+ T cells did not affect infection in IL-13−/− mice. Collectively, these data demonstrate a lack of CD4+ T cell involvement and a novel role for IL-13 in innate responses to infection. We also showed that IL-13 deficiency increased macrophage uptake of Cmu in vitro and in vivo. Moreover, the depletion of IL-13 during infection of lung epithelial cells in vitro decreased the percentage of infected cells and reduced bacterial growth. Our results suggest that enhanced IL-13 responses in the airways, such as that found in asthmatics, may promote susceptibility to chlamydial lung infection. Importantly the role of IL-13 in regulating infection was not limited to the lung as we showed that IL-13 also promoted susceptibility to Cmu genital tract infection. Collectively our findings demonstrate that innate IL-13 release promotes infection that results in enhanced inflammation and have broad implications for the treatment of chlamydial infections and IL-13-associated diseases.
Highlights
Chlamydiae are Gram-negative, obligate intracellular bacteria that commonly cause respiratory and genital tract as well as ocular infections in humans
Chlamydial infections are a common cause of respiratory, genital tract and eye diseases, and infections are clinically associated with the aetiology of asthma, emphysema, heart disease and Alzheimer’s
In this study we have investigated the role of the immune factor, interleukin-13 (IL-13), in C. muridarum infections in mice
Summary
Chlamydiae are Gram-negative, obligate intracellular bacteria that commonly cause respiratory and genital tract as well as ocular infections in humans. Chlamydiae commonly cause asymptomatic infections and significantly, between 50–80% and 10–20% of adults have anti-C. pneumoniae and anti-C. trachomatis antibodies respectively, indicating the high prevalence of these infections within the community [1,6,7,8]. Chlamydial infection has been linked with a number of chronic disease states including asthma [9], chronic obstructive pulmonary disease (COPD) [10,11], atherosclerotic cardiovascular disease [12], and neurodegenerative disorders such as Alzheimer’s disease [13]. Understanding the complex immunobiology of host-pathogen interactions and the delineation of the specific responses that drive clearance versus tissue damage are of paramount importance for the prevention and treatment of chlamydial infection and diseases
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