HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

The regulation of burn-associated infections with herpes simplex virus type 1 or Candida albicans by a non-toxic aconitine-hydrolysate, benzoylmesaconine. Part 2: Mechanism of the antiviral action.

Abstract
In the accompanying paper, the resistance to infections with HSV type 1 (HSV-1) and Candida albicans was improved in thermally injured mice treated with benzoylmesaconine (BEN), an aconitine-hydrolysate isolated from heated Aconiti tuber, or inoculated with splenic CD4+ T cells from BEN-treated mice (BEN T cells). In this paper, therefore, the antiviral mechanism of BEN T cells (or BEN) on the improved resistance of burned mice to the HSV-1 infection was studied. Burn-associated CD + CD11b+ TCRgamma/delta+ type-2 T cells have been shown to be a key on the increased susceptibility of thermally injured mice to infection with HSV-1 or C. albicans. The susceptibility of T6S-mice, mice inoculated with 1 x 10(6) cells/mouse of T6S cells (a clone of burn-associated type-2 T cells), to HSV-1 infection was similar to that of thermally injured mice. The adoptive transfer of BEN T cells to T6S-mice restores their impaired resistance to HSV-1 infection. The type-2 cytokine levels in sera of T6S-mice were decreased after inoculation of BEN T cells. BEN T cells inhibited the type-2 cytokine production by T6S cells when they were cocultured in vitro. BEN T cells, characterized as CD4+ CD28+ TCRalpha/beta+ Vicia villosa (VV) lectin-adherent T cells, showed non-specific ability to inhibit the cytokine production by various type-2 T cells. From the results of the cytokine-producing profile, BEN T cells were shown to be a different subset of CD4+ T cells from Th1 and Th2 cells, although these three CD4+ T cells had similar properties phenotypically. BEN T cells were induced in normal mice 1-4 days after the oral treatment of BEN (1 microg/kg or more). These results suggest that, through the induction of antagonistic CD4+ T cells against burn-associated type-2 T cells, BEN may improve the resistance of T6S-mice (or thermally injured mice) to the infection of HSV-1.
AuthorsM Kobayashi, H Kobayashi, K Mori, R Pollard, F Suzuki
JournalImmunology and cell biology (Immunol Cell Biol) Vol. 76 Issue 3 Pg. 209-16 (Jun 1998) ISSN: 0818-9641 [Print] United States
PMID9682964 (Publication Type: Journal Article)
Chemical References
  • Cytokines
  • benzoylmesaconine
  • Aconitine
Topics
  • Aconitine (analogs & derivatives, therapeutic use)
  • Animals
  • Burns (complications, microbiology, virology)
  • CD4-Positive T-Lymphocytes (drug effects, immunology, metabolism)
  • Candida albicans (drug effects, growth & development)
  • Candidiasis (etiology, prevention & control)
  • Clone Cells (drug effects, virology)
  • Cytokines (biosynthesis)
  • Disease Susceptibility
  • Herpes Simplex (etiology, prevention & control)
  • Herpesvirus 1, Human (drug effects, growth & development)
  • Hydrolysis
  • Immunophenotyping
  • Lymphocyte Activation (drug effects)
  • Mice
  • Mice, Inbred BALB C
  • T-Lymphocyte Subsets (drug effects, immunology, metabolism)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: