Prevention of death in bacterium-infected mice by a synthetic antimicrobial peptide, L5, through activation of host immunity
| Autor: | Nobuko Akiyama, Giichi Sugimori, Shunji Natori, Yukiko Okuyama-Nishida, Koichi J. Homma, Kazuhide Nomura, Kazuhisa Sekimizu, Kenji Ogawa, Masafumi Tsujimoto |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Chemokine
medicine.disease_cause Chemokine CXCL9 Enterococcus faecalis Neutrophil Activation Microbiology Mice Immune system In vivo Immunity medicine Animals Pharmacology (medical) Experimental Therapeutics Pharmacology Mice Inbred ICR biology Dose-Response Relationship Drug Stereoisomerism Bacterial Infections Macrophage Activation Antimicrobial biology.organism_classification Anti-Bacterial Agents Infectious Diseases Staphylococcus aureus Immunology biology.protein CXCL9 Female Reactive Oxygen Species Oligopeptides Injections Intraperitoneal |
| Zdroj: | Antimicrobial agents and chemotherapy. 53(6) |
| ISSN: | 1098-6596 |
| Popis: | In our previous study, we found that the antibacterial peptide KLKLLLLLKLK-NH2(L5) and itsd-enantiomer (DL5) activate neutrophils to produce superoxide anions (O2−) and prevent death due to infection by methicillin-resistantStaphylococcus aureus, suggesting that these peptides may elicit in vivo antimicrobial activities through host inflammatory responses mediated by neutrophils. In this study, we investigated the mechanisms behind in vivo antimicrobial prophylaxis by the use of L5 for the treatment of bacterial infection introduced via intra-abdominal implantation. We found that the intraperitoneal treatment with L5 before bacterial infection markedly reduced rates of death due to infection. Treatments with L5 were highly effective in preventing death due to intraperitoneal inoculation of not onlyS. aureusSmith but alsoEnterococcus faecalisSR1004 andEscherichia coliEC14. The intra-abdominal administration of L5 induced accumulation of neutrophils, increased levels of reactive oxygen species, and augmented antibacterial activity in the abdominal cavity. In addition, administration of L5 upregulated the expression of theMig/CXCL9chemokine gene in thioglycolate-elicited peritoneal macrophages. Our results suggested that the prevention of death by treatment of infected mice with L5 might occur primarily through the activation of a host immune response. |
| Databáze: | OpenAIRE |
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