Methyl gallate limits infection in mice challenged with Brucella abortus while enhancing the inflammatory response
Issue Date
3-2016
Abstract
To investigate the effects of methyl gallate (MG) on murine macrophages, cytokine production and treatment of Brucella abortus infection using a mouse model. Methods and Results: MG-treated cells displayed increased F-actin polymerization and modest increase in ERK, JNK and p38α phosphorylation levels. The mice were intraperitoneally infected with Br. abortus and were orally treated with PBS or MG for 14 days. The weight and bacterial number from each spleen were monitored, and the serum was evaluated for cytokine production. The spleen proliferation and bacterial burden were lower in the MG-treated group than in the MG-untreated control. The noninfected MG-treated mice displayed increased production of TNF, IFN-γ, and the chemokine MCP-1, whereas the Br. abortus-infected MG-treated mice revealed enhanced induction of IL-12p70, TNF and IL-10 compared to the MG-untreated control. Conclusions: MG induced F-actin polymerization and modest upregulation of MAPKs. Furthermore, oral treatment with MG induced an immune response and decreased bacterial proliferation in Br. abortus-infected mice, suggesting that MG may be an alternative treatment for brucellosis. Significance and Impact of the Study: The present study demonstrates the therapeutic effects of MG against Brucella infection through induction of cytokine production and protection from bacterial proliferation in the spleens of mice.
Source or Periodical Title
Journal of Applied Microbiology
ISSN
1364-5072
Volume
120
Issue
3
Page
552-559
Document Type
Article
Physical Description
illustrations, graphs
Language
English
Subject
Brucella abortus, Cytokines, F-actin, Methyl gallate, Mitogen-activated protein kinases
Recommended Citation
Reyes, A.W.B., Kim, D.G., Simborio, H.L.T., Hop, H.T., Arayan, L.T., Min, W., Lee, J.J., Chang, H.H., Kim, S. (2015). Methyl gallate limits infection in mice challenged with Brucella abortus while enhancing the inflammatory response. Journal of Applied Microbiology, 120 (3), 552-559. DOI: 10.1111/jam.13019.
Identifier
doi: 10.1111/jam.13019.
Digital Copy
yes