Depressed production of beta-defensins from mouse splenic dendritic cells following thermal injury and its influence on susceptibility to infection

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• 作者：Takashi Kawasaki ; Chika Kawasaki ; Takeyoshi Sata ; Makiko Kobayashi…
• 关键词：Burn ; Defensin ; Dendritic cell ; Infection ; Innate immunity ; Host defense
• 刊名：Journal of Anesthesia
• 出版年：2015
• 出版时间：February 2015
• 年：2015
• 卷：29
• 期：1
• 页码：78-86
• 全文大小：416 KB
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• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Anesthesiology
  
• 出版者：Springer Japan
• ISSN：1438-8359

文摘

Purpose 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 normal mice and full-thickness (FT)-burned mice. Methods DCs were isolated from spleens of mice, and 1?×?106 cells/ml of them were cultured with LPS or SAC. Culture fluids harvested 24?h after cultivation were assayed for BD1 and BD3 and antibacterial activity (colony-counting, Pseudomonas aeruginosa). Also, DCs were tested for BD mRNAs by RT-PCR. Results Sixty-five percent of the bacterial killing activity was shown by the culture fluids of splenic DC from normal mice, while only 15?% killing activity was shown by the culture fluids of splenic DC from FT-burned mice. X-irradiated NOD SCID IL-2rγnull mice inoculated with splenic DC from FT-burned mice showed increased susceptibility to P. aeruginosa infection compared to those from normal mice. Mice splenic DC expressed BD1 mRNA constitutively and expressed BD3 mRNA after stimulation. These BDs were produced by mice splenic DC. As compared with DC from normal mice, DC from FT-burned mice produced decreased amounts of BD1 and BD3 in their culture fluids. Conclusions 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 FT-burned mice are susceptible to P. aeruginosa infection, BDs produced by DC may play an important role on the host’s antibacterial resistance.