A highly susceptible CD46 transgenic mouse model of subcutaneous infection with Streptococcus dysgalactiae subspecies equisimilis

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• 作者：Haruno Yoshida^a ; Tetsufumi Takahashi^b ; Masahiko Nakamura^b ; Anders Ø ; verby^b ; Takashi Takahashi^a ; Kimiko Ubukata^a ; ¹ ; Hidenori Matsui^a ; ^{hmatsui@lisci.kitasato-u.ac.jp" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Streptococcus dysgalactiae subsp. equisimilis ; Streptococcal toxic shock syndrome ; CD46 transgenic mouse ; Pyogenic abscess ; Necrotic lesion ; Ankle arthritis
• 刊名：Journal of Infection and Chemotherapy
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：22
• 期：4
• 页码：229-234
• 全文大小：1488 K

文摘

The Streptococcus dysgalactiae subspecies equisimilis (SDSE) possesses clinical similarities to group A streptococcus (GAS) and has recently been recognized as a causative pathogen of life-threatening streptococcal infections. Human membrane cofactor protein (CD46), a complement regulatory protein ubiquitously expressed on every cell type except for erythrocytes, has been implicated as a receptor for human-specific pathogens including GAS. In the present report, SDSE strain GGS_124 was isolated from a patient suffering from streptococcal toxic shock syndrome. When CD46-expressing transgenic (Tg) and non-Tg mice were infected subcutaneously into a hind footpad with 1 × 10⁷ colony-forming units of GGS_124, both CD46 Tg and non-Tg mice showed similar levels of colonization in the popliteal lymph nodes at day 3 after infection. However, the following differences were found between CD46 Tg and non-Tg mice after infection. First, there was a statistically significant difference in mortality rates between CD46 Tg (33%) and non-Tg (0%) mice within 35 days after infection. Second, all surviving CD46 Tg mice developed ankle arthritis at day 35 after infection, whereas non-Tg mice did not develop ankle arthritis on the infected hind paws. Finally, CD46 Tg mice developed a pus-filled abscess accompanied by renal failure at day 6 or later after infection. These observations suggest that CD46, the host cell-surface pathogen receptor, functioned to attract GGS_124 into deep tissues, so that the subcutaneous infection with GGS_124 induced invasive streptococcal diseases in CD46 Tg mice.