The antibacterial activity and toxin production control of bee venom in mouse MRSA pneumonia model.
A549 Cells
Animals
Anti-Bacterial Agents
/ pharmacology
Anti-Inflammatory Agents
/ pharmacology
Apitherapy
Bee Venoms
/ pharmacology
Disease Models, Animal
Female
Gene Expression
/ drug effects
Humans
Methicillin-Resistant Staphylococcus aureus
/ drug effects
Mice
Mice, Inbred BALB C
Microbial Sensitivity Tests
Pneumonia, Staphylococcal
/ drug therapy
RAW 264.7 Cells
Republic of Korea
Bee venom
MRSA
Pneumonia
Toxin
Journal
BMC complementary medicine and therapies
ISSN: 2662-7671
Titre abrégé: BMC Complement Med Ther
Pays: England
ID NLM: 101761232
Informations de publication
Date de publication:
27 Jul 2020
27 Jul 2020
Historique:
received:
20
05
2019
accepted:
16
06
2020
entrez:
29
7
2020
pubmed:
29
7
2020
medline:
23
1
2021
Statut:
epublish
Résumé
The current antimicrobial therapy is still important for the treatment of pneumonia due to MRSA infection, but there are some limitations, including the route of administration, side effect profile, and increased microbial resistance patterns. Therefore, we investigated whether BV, which shows a strong antimicrobial effect against MRSA, would be effective in a pneumonia model. In vitro, we checked MIC, qRT-PCR, western blot, ELISA, LDH-assay. In vivo, we checked survival rate, gross pathological change, histopathology, lung bacterial clearance assay, and the expression of inflammatory related gene. The minimum inhibitory concentration of BV against MRSA is 15.6 μg/ml by broth dilution method. The production of toxins and related gene were reduced by BV in MRSA. The secretion of cytokines were decreased by treatment with BV in 264.7 RAW macrophages stimulated by MRSA Also, BV protected A549 from pathogenicity of MRSA. Bee venom reduced the number of bacteria in the lungs and alleviated the symptoms of MRSA-induced pneumonia in mouse. BV inhibited the virulence of the bacterium and the number of bacterial cells present in lung tissue, thereby alleviating the symptoms of pneumonia in mice. This study suggested that BV may be a candidate substance for the treatment of pneumonia caused by MRSA infection.
Sections du résumé
BACKGROUND
BACKGROUND
The current antimicrobial therapy is still important for the treatment of pneumonia due to MRSA infection, but there are some limitations, including the route of administration, side effect profile, and increased microbial resistance patterns. Therefore, we investigated whether BV, which shows a strong antimicrobial effect against MRSA, would be effective in a pneumonia model.
METHODS
METHODS
In vitro, we checked MIC, qRT-PCR, western blot, ELISA, LDH-assay. In vivo, we checked survival rate, gross pathological change, histopathology, lung bacterial clearance assay, and the expression of inflammatory related gene.
RESULTS
RESULTS
The minimum inhibitory concentration of BV against MRSA is 15.6 μg/ml by broth dilution method. The production of toxins and related gene were reduced by BV in MRSA. The secretion of cytokines were decreased by treatment with BV in 264.7 RAW macrophages stimulated by MRSA Also, BV protected A549 from pathogenicity of MRSA. Bee venom reduced the number of bacteria in the lungs and alleviated the symptoms of MRSA-induced pneumonia in mouse.
CONCLUSION
CONCLUSIONS
BV inhibited the virulence of the bacterium and the number of bacterial cells present in lung tissue, thereby alleviating the symptoms of pneumonia in mice. This study suggested that BV may be a candidate substance for the treatment of pneumonia caused by MRSA infection.
Identifiants
pubmed: 32718325
doi: 10.1186/s12906-020-02991-8
pii: 10.1186/s12906-020-02991-8
pmc: PMC7385961
doi:
Substances chimiques
Anti-Bacterial Agents
0
Anti-Inflammatory Agents
0
Bee Venoms
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
238Subventions
Organisme : the Basic Science Research Program through the National Research Foundation (NRF) of Korea funded by the Ministry of Education
ID : NRF-2016R1D1A1B03934552
Organisme : the National Research Foundation of Korea (NRF) grant funded by the Korea government(MSIT)
ID : NRF-2017R1A2B1009979
Commentaires et corrections
Type : ErratumIn
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