201. A deep-sea pathogenic Bacillus subtilis isolate employs different strategies to escape the killing of teleost and murine complements
- Author
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Mo-fei Li, Li Sun, and Han-jie Gu
- Subjects
0301 basic medicine ,Immunology ,Blotting, Western ,Flounder ,Enzyme-Linked Immunosorbent Assay ,Bacillus subtilis ,Bacillaceae Infections ,Biology ,Serum resistance ,Microbiology ,Cell wall ,03 medical and health sciences ,chemistry.chemical_compound ,Fish Diseases ,Mice ,Hydrothermal Vents ,Animals ,Immune Evasion ,Mice, Inbred BALB C ,030102 biochemistry & molecular biology ,Virulence ,Chemotaxis ,Complement System Proteins ,biology.organism_classification ,Olive flounder ,Complement system ,030104 developmental biology ,RAW 264.7 Cells ,chemistry ,Host-Pathogen Interactions ,Lysozyme ,Developmental Biology - Abstract
Bacillus subtilis subsp. subtilis G7 was isolated from a deep-sea hydrothermal vent and is pathogenic to pathogenic to fish (Japanese flounder) and mice. G7 is able to survive in host sera and phagocytes. In this study, we investigated the underlying mechanism of G7 serum resistance. We found that (i) the remaining complement activity was very low in G7-incubated flounder serum but high in G7-incubated mouse serum; (ii) cleaved C3 and C5 components were detected on flounder serum-incubated G7 but not on mouse serum-incubated G7; (iii) abundant uncleaved C5 was localized in G7-incubated mouse, but not flounder, serum; (iv) G7-incubated flounder, but not mouse, serum exhibited strong chemotactic activity; (v) pre-treatment with low-dose lysozyme abolished the serum resistance of G7. Hence, G7 activates flounder complement but is protected from complement-mediated destruction by its cell wall structure, while G7 prevents the activation of mouse complement. These results indicate that G7 employs different mechanisms to avoid the complement killing of different hosts.
- Published
- 2020