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*
Department of Medical Microbiology and Hygiene, University of Ulm, Ulm, Germany; and
Department of Microbiology, University of Rijeka, Rijeka, Croatia
The inflammatory response and influence of T cell depletion on the
pathogenesis of an experimental Legionella infection were
studied. A/J mice were infected with 106 CFU of
Legionella pneumophila intratracheally. With this dose all
infected animals survived the infection and bacteria were cleared from
lung, spleen, liver, and kidney within 10 to 11 days, leaving no
residual changes in the affected organs. Inflammatory cells were
recruited into the lung on the second day of infection, reaching a
maximum on the third day and filling out predominantly the interstitial
areas. During the first 3 days after inoculation, mainly macrophages, B
cells, NK cells, and large mononuclear cells of an unknown phenotype
were attracted into the lung interstitium, whereas T lymphocytes
infiltrated subsequently. During the early phase of infection, serum
concentrations of IFN-
, TNF-
, IL-1ß, IL-4, and IL-6 but not
IL-2 increased dramatically. The cytokine secretion decreased on the
third day after infection although bacteria were still present in the
lung or even disseminated in different organs. Successful clearance of
bacteria from the lung was not observed before recruitment of T cells
into the lung. In mice depleted of both CD4+ and
CD8+ T cells, control of infection was impaired and
lethality of infection increased. Depletion of either subset left
residual antibacterial mechanisms, which, however, were not sufficient
to clear the Legionella as rapidly as in undepleted mice.
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