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Dendritic cells as a producer cell of beta‐defensins
Author(s) -
Kawasaki Takashi,
Kobayashi Makiko,
Herndon David N,
Suzuki Fujio
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.673.12
Subject(s) - chemistry , microbiology and biotechnology , immunology , burn injury , andrology , biology , medicine , surgery
Beta‐defensins (BDs) and dendritic cells (DC) have been described as major effectors on host antimicrobial innate immunities. In the present study, the ability of DC to produce BDs was explored using DC from mice with different severities of burn injuries. FT‐burned mice (BALB/c mice with 25% TBSA flame burn, 3 rd degree) and PT‐burned mice (BALB/c mice with 25% TBSA scald burn, 1 to 2 nd degree) were prepared as described previously. DC were isolated from spleens of mice 3 days after burn injuries, and 1×10 6 cells/ml of them were cultured with LPS or SAC. Culture fluids harvested 24 hrs after cultivation were assayed for BD1 and BD3 (ELISA) and a bactericidal activity (colony‐counting, P. aeruginosa ). Also, DC were tested for BD mRNAs by RT‐PCR. 90% of the bacterial growth was inhibited by the culture fluids of splenic DC from PT‐burned mice, while only 30% growth inhibition was shown by the culture fluids of splenic DC from FT‐burned mice. As compared with DC from normal mice, DC from PT‐burned mice produced increased amounts of BD1 and BD3 in their culture fluids, while decreased amounts of BDs were produced by DC from FT‐burned mice. The results were reproduced in 2 different assays for BDs (ELISA and RT‐PCR). These results indicate that 1) DC from spleens of mice have an ability to produce BDs, and 2) the production of BDs by DC is influenced strongly by thermally injured stress. Since PT‐burned mice are resistant and FT‐burned mice are susceptible to P. aeruginosa infection, BDs produced by DC may play an important role on the host's antibacterial resistance. (Supported by SHC NA #8610.)