Open AccessProtection by dexamethasone from a lethal infection with Listeria monocytogenes in mice
Author(s) -
Nakane Akio,
Okamoto Munenori,
Asano Misako,
Kohanawa Masashi,
Satoh Yuichiro,
Minagawa Tomonori
Publication year - 1994
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.1994.tb00487.x
Subject(s) - dexamethasone , endogeny , listeria monocytogenes , biology , ratón , tumor necrosis factor alpha , interferon gamma , cytokine , lethal dose , necrosis , immunology , medicine , endocrinology , toxicology , genetics , bacteria
The effects of dexamethasone (DEX) on a lethal infection with Listeria monocytogenes were studied in mice. Mice were completely protected against the lethal infection when treated with 3.3 mg per kg of DEX. The effect was observed only when DEX was injected before infection. The control mice died from day 3 to day 5 of infection, whereas DEX‐treated mice could eliminate L. monocytogenes cells from the organs by day 11 of infection. High titres of endogenous tumour necrosis factor (TNF), interleukin‐6 (IL‐6) and gamma interferon (IFN‐γ) were induced in the bloodstreams and organs of the drug‐free mice. DEX suppressed IL‐6 production, but augmented TNF and IFN‐γ production within 24 h of infection, whereas production of all three endogenous cytokines was suppressed in the DEX‐treated mice on day 3 of infection when the control mice began to die. These results suggest that DEX shows a protective effect on a lethal infection with L. monocytogenes in mice and that regulation of production of endogenous cytokines might be involved in the effect of DEX.