We examined the effects of temperature on the interaction between
Legionella pneumophila and phagocytes of guinea pigs. The body temperatures of guinea pigs infected with a sublethal dose (1.2×10
4 CFU) or a lethal dose (1.0×10
5 CFU) of
L. pneumophila elevated from 38.4±0.15C to 40.2±0.42C or 40.3 ±0.62C, respectively. The intracellular bacterial killing by and bacterial proliferation in the phagocytes were examined at 33, 37, 40, and 42C, using
in vitro culture systems of peritoneal macrophages or polymorphonuclear leukocytes (PMN) of guinea pigs. In all the macrophages incubated at different temperatures, significant intracellular bacterial killings were observed at 4hr after
in vitro phagocytosis. After 24hr of incubation, there was about a 100-fold increase of CFU and the number reached a maximum after 48hr of incubation in the macrophages incubated at 42C as well as 37 and 40C, suggesting that macrophages support the intracellular bacterial growth in hyperthermia. In the PMN,
L. pneumophila CFU 4hr or 12hr after the infection were significantly lower at 42C than those at 37C (
P<0.05), indicating that the bactericidal capacity of PMN was enhanced at 42C compared to 37C. However, in all the PMN incubated at different temperatures, there were about 10-fold increases of CFU 24hr after the infection, suggesting that PMN as well as macrophages support intracellular bacterial growth in hyperthermia. The extracellular bacterial growth was examined at 33, 37, 40, and 42C in buffered yeast extract (BYE) broth or RPMI 1640 medium containing 50% guinea pig serum as a permissive or non-permissive liquid medium for the bacterial growth, respectively. Inhibition of bacterial growth in BYE broth at 42C, and a decrease of CFU in RPMI 1640 medium containing 50% guinea pig serum at 42C were observed. In conclusion, hyperthermia may be beneficial by restricting extracellular bacterial survival, but it exerts no beneficial effect on the restriction of intracellular bacterial growth in phagocytes, though PMN showed enhanced initial killing at 42C. These results suggest that fever, or hyperthermia itself, may not largely contribute as a nonspecific host defense early in the course of legionellosis.
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