A soluble form of Siglec-9 provides a resistance against Group B Streptococcus (GBS) infection in transgenic mice

Mitsumasa Saito, Sayo Yamamoto, Kinuyo Ozaki, Yukiko Tomioka, Haruka Suyama, Masami Morimatsu, Ken ichi Nishijima, Shin ichi Yoshida, Etsuro Ono

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Abstract

Group B Streptococcus (GBS) is a leading cause of invasive bacterial infections in human newborns. A key GBS virulence factor is its capsular polysaccharide (CPS), possessing terminal sialic acid residues that suppress host immune response and provide a survival advantage to the pathogen. CPS binds to Siglec-9 expressed on neutrophils, which is expected to down-regulate the immune responsiveness of neutrophils. We hypothesized that a soluble form of Siglec-9 (sSiglec-9) competitively inhibits a binding of CPS to Siglec-9 on immune cells, leading to provide antibacterial benefit against GBS infection in the transgenic mouse line expressing sSiglec-9 (sSiglec-9 Tg). The sSiglec-9 in the sera of sSiglec-9 Tg bound to the sialylated-GBS strains belonging to serotypes Ia, Ib, II, III, IV and V in whole GBS cell ELISA. When GBS cells of serotype III that is a common serotype in late-onset GBS disease (LOD) were intraperitoneally inoculated into sSiglec-9 Tg, sSiglec-9 Tg showed a significant resistance as compared with non-transgenic littermates. Furthermore, GBS serotype III organisms were not detected in cultures of the blood from surviving mice (<1 × 103 CFU/ml). These results indicated that sSiglec-9 Tg mice were more efficient in eliminating GBS and survived better after the intraperitoneal challenge with GBS serotype III bacteria.

Original languageEnglish
Pages (from-to)106-110
Number of pages5
JournalMicrobial Pathogenesis
Volume99
DOIs
Publication statusPublished - Oct 1 2016

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Infectious Diseases

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    Saito, M., Yamamoto, S., Ozaki, K., Tomioka, Y., Suyama, H., Morimatsu, M., Nishijima, K. I., Yoshida, S. I., & Ono, E. (2016). A soluble form of Siglec-9 provides a resistance against Group B Streptococcus (GBS) infection in transgenic mice. Microbial Pathogenesis, 99, 106-110. https://doi.org/10.1016/j.micpath.2016.08.014