The 94th Annual Meeting of Japanese Society for Bacteriology

Presentation information

On-demand Presentation

6 Virulence Factors and Biophylaxis

[ODP6E] e. Basic Studies using Infection Model

[ODP-162] Hyaluronate Lyase Involved in Nutrient Acquisition and Pathogenicity of Streptococcus dysgalactiae

○An Van Nguyen1, Kohei Ogura2, Miki Matsue3, Norihiko Takemoto4, Wataru Hashimoto5, Shigefumi Okamoto3, Hiroshi Ichimura1 (1Dept. Viral Infect., Grad. Sch. Med. Sci., Kanazawa Univ., 2Inst. Front. Sci. Init., Kanazawa Univ., 3Dept. Clin. Lab. Sci., Inst. Med. Pharm. Health Sci., Kanazawa Univ., 4Pathog. Microb. Lab., Res. Inst., NCGM, 5Lab. Bas. Appl. Mole. Biotech., Div Food Sci. Biotech., Grad. Agric., Kyoto Univ.)

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.