Crucial role of IFN-gamma receptor in murine Legionella longbeachae infection
Abstract number: P959
Gobin I., Selenic K., Trobonjaca Z., Doric M., Susa M.
Objectives:Legionella longbeachae serogroup 1, a facultative intracellular pathogen is a causative agent of life-threatening pneumonia. Human infection is particulary common in Australia, but sporadic infections have been documented in other countries. Previous studies have shown that activation of U937 macrophages with interferon-gamma (IFN-g) restricts the growth of L. longbeachae. In this study we decided to explore the role of IFN-g receptor in L. longbeachae mice infection. We explored the kinetics of bacterial multiplication and patohistological changes in IFN-gR -/- knock out and C57Bl/6 mice.
Methods: Pathogen-free 6- to 10-weeks-old IFN-gR -/- and C57Bl/6 (control) mice were infected by intratracheal inoculation with L. longbeachae serogroup 1 (clinical isolate D4968) using a dose of 103 CFU. We determined the mortality rate and bacterial clearence from the lungs of infected mice at different time points post infection. We also followed the patohistological changes in these organs during 72 hours of infection.
Results: Our results showed a dramatic difference in the mortality rate between IFN-gR -/- and control C57Bl/6 mice. After intratracheal infection with 103 CFU of L. longbeachae all IFN-gR -/- mice died within 5 days, while control mice survived the infection. Mice infected with 103 CFU of L. longbeachae were not able to overcome infection for more than 5 days. In contrast, control mice could reduce the bacterial burden in the lungs below the assay detection level 14 days p.i. They, however, showed focal peribronchiolar inflammatory cell infiltration with basement membrane injury, three to seven days after infection. On the other hand, IFN-gR -/- mice developed severe bronchopneumonia with destruction of the alveolar wall and infiltration of the interstitial tissue within neutrophils and lymphocytes three days after infection.
Conclusion: Our results shows that IFN-g receptor plays a crucial role in the host defence against L. longbeachae serogroup 1 infection. The findings suggest that retardation of the host immune response caused by deficiency of IFN-gR, might allow bacteria to grow and cause fulminant pneumonia.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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