第94回日本細菌学会総会

講演情報

オンデマンド口頭発表(ODP)

6 病原因子と生体防御

[ODP6E] e. 感染モデルを用いた基礎研究

[ODP-162] Streptococcus dysgalactiae の資化性と病原性に関与するヒアルロン酸リアーゼ

○An Van Nguyen1,小倉 康平2,松榮 美希3,竹本 訓彦4,橋本 渉5,岡本 成史3,市村 宏1 (1金沢大院・医・ウイルス感染症,2金沢大・新学術創成研究,3金沢大院・医薬保健・病態検査学,4国立国際医療研究セ・感染症制御・病態微生物,5京都大院・農・食品生物・生物機能変換)

Streptococcus dysgalactiae subsp. equisimilis (SDSE), a β-hemolytic streptococcus, causes a variety of infectious disease such as cellulitis, bacteremia, and severe shock syndrome in humans. SDSE infection is more prevalent among elders or diabetes mellitus patients than infection with Streptococcus pyogenes (GAS) and Streptococcus agalactiae (GBS). The mechanisms underlying the pathogenicity of SDSE were unknown. In this study we evaluated the role of hyaluronate lyase (Hyl) and unsaturated glucuronyl hydrolase (UGL), which degrade hyaluronic acid (HA) and resultant oligosaccharides, respectively, in the pathogenicity of SDSE.
The expression levels of genes encoding Hyl and UGL were higher than those in GBS. SDSE Hyl retained enzymatic activity at pH 6.0. We found that the deletion of hyl gene decreased in mortality among SDSE-infected mice. The wild-type (WT) SDSE cells, but not hyl-deleted SDSE (MT) cells, were observed at the infected wounds with intensive infiltration of neutrophils on day 2 post-infection. Serum IL-6 concentrations were higher in WT SDSE-infected mice than in MT SDSE-infected mice. In the presence of HA as a sole nutrition source, SDSE grew and divided rapidly than GBS and GAS. Our study suggested that Hyl and UGL of SDSE play important roles in nutrient acquisition from hosts, followed by the bacterial pathogenicity damaging host tissues.