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タイトル: Involvement of beta-defensin 130 (DEFB130) in the macrophage microbicidal mechanisms for killing Plasmodium falciparum
著者: Terkawi, Mohamad Alaa
Takano, Ryo
Furukawa, Atsushi
Murakoshi, Fumi
Kato, Kentaro
発行日: 9-Feb-2017
出版者: Nature Publishing Group
誌名: Scientific Reports
巻: 7
開始ページ: 41772
抄録: Understanding the molecular defense mechanism of macrophages and identifying their effector molecules against malarial parasites may provide important clues for the discovery of new therapies. To analyze the immunological responses of malarial parasite-induced macrophages, we used DNA microarray technology to examine the gene profile of differentiated macrophages phagocytizing Plasmodium falciparum-parasitized erythrocytes (iRBC). The transcriptional gene profile of macrophages in response to iRBCs represented 168 down-regulated genes, which were mainly involved in the cellular immune response, and 216 upregulated genes, which were involved in cellular proteolysis, growth, and adhesion. Importantly, the specific upregulation of beta-defensin 130 (DEFB130) in these macrophages suggested a possible role for DEFB130 in malarial parasite elimination. Differentiated macrophages phagocytizing iRBCs exhibited an increase in intracellular DEFB130 levels and DEFB130 appeared to accumulate at the site of iRBC engulfment. Transfection of esiRNA-mediated knockdown of DEFB130 into macrophages resulted in a remarkable reduction in their antiplasmodial activity in vitro. Furthermore, DEFB130 synthetic peptide exhibited a modest toxic effect on P. falciparum in vitro and P. yoelii in vivo, unlike scrambled DEFB130 peptide, which showed no antiplasmodial activity. Together, these results suggest that DEFB130 might be one of the macrophage effector molecules for eliminating malarial parasites. Our data broaden our knowledge of the immunological response of macrophages to iRBCs and shed light on a new target for therapeutic intervention.
URI: http://ir.obihiro.ac.jp/dspace/handle/10322/4448
DOI: info:doi/10.1038/srep41772
ISSN: 2045-2322
権利情報: This is an open access article licensed under the terms of the Creative Commons Attribution (by) License. <http://creativecommons.org/lisenses/by/4.0/>
出現コレクション:05001学術雑誌論文

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