Open AccessCharacterization of sugar recognition by the toxin complex produced by the Clostridium botulinum serotype C variant strain Yoichi
Author(s) -
Matsuo Tomohito,
Miyata Keita,
Inui Ken,
Ito Hiroaki,
Horiuchi Ryohta,
Suzuki Tomonori,
Yoneyama Tohru,
Oguma Keiji,
Niwa Koichi,
Watanabe Toshihiro,
Ohyama Tohru
Publication year - 2011
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2011.00825.x
Subject(s) - neuraminidase , lactose , strain (injury) , biochemistry , galactose , sialic acid , chemistry , microbiology and biotechnology , biology , anatomy , enzyme
Clostridium botulinum serotype C strains produce a neurotoxin (BoNT) along with nontoxic proteins, including nontoxic nonhemagglutinin and three hemagglutinin subcomponents, HA‐70, HA‐33 and HA‐17, to form a large toxin complex (L‐TC). While L‐TCs produced by serotype C strains usually exhibit hemagglutination (HA) activity via HA‐33 binding to sialic acid on erythrocytes, serotype C strain Yoichi (C‐Yoichi) L‐TC exhibited neither HA nor binding activity towards erythrocytes, probably due to a C‐terminal truncation of the HA‐33 protein. However, here, we demonstrate that C‐Yoichi L‐TC newly showed full HA and binding activity towards neuraminidase‐treated erythrocytes that was completely inhibited in the presence of galactose (Gal) or lactose (Lac). Binding of C‐Yoichi L‐TC to rat small intestine epithelial cells (IEC‐6) treated with neuraminidase was also significantly enhanced compared with untreated IEC‐6 cells. Similarly, the HA‐33/HA‐17 complex isolated from C‐Yoichi L‐TC also bound to neuraminidase‐treated IEC‐6 cells. The binding activity of both L‐TC and HA‐33/HA‐17 was inhibited in the presence of Gal or Lac. Additionally, C‐Yoichi L‐TC adsorbed tightly to a lactose‐affinity gel column. These results strongly suggest that the unusual recognition of the Gal moiety on the cells could be due to a variation and/or a truncation in the C‐terminal‐half of the unique C‐Yoichi HA‐33 protein.