The antibacterial activity and toxin production control of bee venom in mouse MRSA pneumonia model
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(2020) 20:238
RESEARCH ARTICLE
BMC Complementary Medicine and Therapies
Open Access
The antibacterial activity and toxin production control of bee venom in mouse MRSA pneumonia model Ryong Kong1, Young-Seob Lee2, Dam-Hee Kang1, Shu Wang1, Qianqian Li1, Dong-Yeul Kwon1 and Ok-Hwa Kang1*
Abstract 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: 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: 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: 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. Keywords: MRSA, Bee venom, Toxin, Pneumonia
Background MRSA is a common cause of nosocomial pneumonia and healthcare-associated pneumonia [1]. The main cause of MRSA-induced pneumonia is toxin. The αhemolysin, a member of the β-barrel pore-forming toxin family, is the major virulence factor secreted by strains of S. aureus [2]. The α-hemolysin is necessary for the pathogenesis of staphylococcal pneumonia. Bubeck Wardenburg et al. have reported that S. aureus mutants * Correspondence: [email protected] 1 Department of Oriental Pharmacy, College of Pharmacy and Wonkwang-Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk 54538, Republic of Korea Full list of author information is available at the end of the article
lacking hla (the gene encoding α-hemolysin) cannot cause neutrophil-mediated inflammatory lung injury in pneumonia model [3]. Similar to most staphylococcal extracellular proteins, the α-toxin is not expressed constitutively but is tightly controlled by an array of extracellular and intracellular signals. At least three global regulatory loci the accessory gene regulator (agr), the staphylococcal accessory gene regulator (sarA), and the staphylococcal accessory protein effector (sae) appear to coordinately control the hla expression in S. aureus in vitro. In addition, two sarA homologs, rot and sarT, repress the hla expression. The agr locus affects
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