Effects of glycyrrhizin, an active component of licorice roots, on Candida albicans infection in thermally injured mice.
Due to the generation of burn-associated CD8+ CD11b+ TCR gamma/delta+ type 2 T cells (burn-associated type 2 T cells), the susceptibility of thermally injured mice to infection with C. albicans has been shown to be increased by up to 50-fold when compared with normal mice. Glycyrrhizin (GR), an active component of licorice roots, reduced the susceptibility of thermally injured mice to C. albicans infection to levels observed in normal mice. Thermally injured mice inoculated with CD4+ T cells from GR-treated mice were also resistant to C. albicans infection. The following demonstrated that susceptibility to fungal infection was similar in thermally injured mice and normal mice inoculated with T6S cells (a clone of burn-associated type 2 T cells). This susceptibility of T6S mice (normal mice inoculated with T6S cells) was reversible by (i) administration of GR, (ii) inoculation of CD4+ T cells from GR-treated mice, and (iii) injection of a mixture of MoAbs targeted against type 2 cytokines (IL-4 and IL-10). After stimulation with anti-CD3 MoAb, splenic T cells from thermally injured and T6S mice, treated with GR or inoculated with CD4+ T cells from GR-treated mice, did not have type 2 cytokines in culture supernatants. They were present in splenic T cell cultures from thermally injured and T6S mice that were treated with saline or inoculated with naive T cells. These results suggest that GR, by inducing CD4+ T cells which suppress type 2 cytokines produced by burn-associated type 2 T cells, improves the resistance of thermally injured mice to C. albicans. An anti-type 2 T cell action of the CD4+ T cells derived from GR-treated mice was previously described.
Utsunomiya
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T
Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555-0835, USA.
Kobayashi
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M
Herndon
D N
DN
Pollard
R B
RB
Suzuki
F
F
D000666:Amphotericin B / Q000494:pharmacology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D000911:Antibodies, Monoclonal / Q000276:immunology; D002056:Burns / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002176:Candida albicans / Q000187:drug effects; D002177:Candidiasis / Q000276:immunology*; D016207:Cytokines / Q000502:physiology; D019695:Glycyrrhizic Acid / Q000494:pharmacology*; D051379:Mice; D008807:Mice, Inbred BALB C
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D016207:Cytokines; D019695:Glycyrrhizic Acid; D000666:Amphotericin B