細菌感染に対する生体の防御機構と細菌毒素による自然免疫機構の障害

DOI Web Site Web Site PubMed 参考文献13件 オープンアクセス

書誌事項

タイトル別名
  • Host Defense against Bacterial Infection and Bacterial Toxin-induced Impairment of Innate Immunity
  • Review for award 細菌感染に対する生体の防御機構と細菌毒素による自然免疫機構の障害
  • Review for award サイキン カンセン ニ タイスル セイタイ ノ ボウギョ キコウ ト サイキン ドクソ ニ ヨル シゼン メンエキ キコウ ノ ショウガイ

この論文をさがす

抄録

<p>　Whereas granulopoiesis during Gram-negative bacterial infection is accelerated through activation of toll-like receptor 4 (TLR4), it has not been elucidated whether Gram-positive bacterial infection can stimulate granulopoiesis. Using the well-known TLR2 agonist peptidoglycan (PGN), it was shown that neutrophils in bone marrow and spleen and plasma granulocyte colony-stimulating factor were increased in mice that had received intraperitoneal administration of PGN. Incorporation of bromodeoxyuridine into bone marrow neutrophils increased in mice administered PGN, demonstrating that PGN promotes granulopoiesis. These results illustrate that bacterial recognition by TLR2 facilitates granulopoiesis during Gram-positive bacterial infection. Thus, granulopoiesis is accelerated to suppress bacterial infection, but some bacteria can still cause severe infections. Clostridium perfringens is a Gram-positive, anaerobic pathogenic bacterium and causes life-threatening gas gangrene in humans. Of the many toxins produced by C. perfringens, α-toxin is known to be a major virulence factor during infection. Recently, it has been revealed that C. perfringens α-toxin impairs the innate immune system by inhibiting neutrophil differentiation, which is crucial for the pathogenesis of C. perfringens. Moreover, the toxin also attenuates erythropoiesis, which would cause severe anemia in clinical settings. The findings provide new insight to understand how hosts strengthen innate immunity to fight pathogenic bacteria and how they evade the hosts' immune systems.</p>

収録刊行物

  • 薬学雑誌

    薬学雑誌 138 (10), 1249-1253, 2018-10-01

    公益社団法人 日本薬学会

参考文献 (13)*注記

もっと見る

関連プロジェクト

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ