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Induction of acute silkworm hemolymph melanization by Staphylococcus aureus treated with peptidoglycan-degrading enzymes.
Matsumoto, Yasuhiko; Sato, Eri; Sugita, Takashi.
Affiliation
  • Matsumoto Y; Department of Microbiology, Meiji Pharmaceutical University, Tokyo, 204-8588, Japan.
  • Sato E; Department of Microbiology, Meiji Pharmaceutical University, Tokyo, 204-8588, Japan.
  • Sugita T; Department of Microbiology, Meiji Pharmaceutical University, Tokyo, 204-8588, Japan.
Drug Discov Ther ; 18(3): 194-198, 2024 Jul 09.
Article in En | MEDLINE | ID: mdl-38925960
ABSTRACT
Staphylococcus aureus, a Gram-positive bacterium, causes inflammatory skin diseases, such as atopic dermatitis, and serious systemic diseases, such as sepsis. In the skin and nasal environment, peptidoglycan (PGN)-degrading enzymes, including lysozyme and lysostaphin, affects S. aureus PGN. However, the effects of PGN-degrading enzymes on the acute innate immune-inducing activity of S. aureus have not yet been investigated. In this study, we demonstrated that PGN-degrading enzymes induce acute silkworm hemolymph melanization by S. aureus. Insoluble fractions of S. aureus treated with lysozyme, lysostaphin, or both enzymes, were prepared. Melanization of the silkworm hemolymph caused by the injection of these insoluble fractions was higher than that of S. aureus without enzyme treatment. These results suggest that structural changes in S. aureus PGN caused by PGN-degrading enzymes affect the acute innate immune response in silkworms.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Bombyx / Staphylococcus aureus / Peptidoglycan / Hemolymph / Muramidase / Immunity, Innate Limits: Animals Language: En Journal: Drug Discov Ther Year: 2024 Document type: Article Affiliation country: Country of publication:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Bombyx / Staphylococcus aureus / Peptidoglycan / Hemolymph / Muramidase / Immunity, Innate Limits: Animals Language: En Journal: Drug Discov Ther Year: 2024 Document type: Article Affiliation country: Country of publication: