Report an error   


Submitted: 24 February 2017 Modified: 03 March 2017
HERDIN Record #: PCHRD17022410515368

Nocodazole treatment interrupted Brucella abortus invasion in RAW 264.7 cells, and successfully attenuated splenic proliferation with enhanced inflammatory response in mice.

Suk Kim,
Hong Hee  Chang,
Hu Jang  Lee,
Wongi Min,
Tran Xuan Ngoc  Huy,
Lauren T. Arayan,
Huynh Tan  Hop,
Alisha Wehdnesday  B. Reyes

See More

Brucellosis is one of the most important and widespread zoonosis worldwide responsible for serious economic losses and considerable public health burden. In this study, we investigated the modulatory effect of a microtubule-inhibitor, nocodazole, on B. abortus infection in murine macrophages and in a mouse model. Nocodazole activated macrophages and directly inhibited the growth of Brucella in a dose-dependent manner. Nocodazole increased adhesion but reduced invasion and intracellular growth of Brucella in macrophages although it did not affect co-localization of Brucella with LAMP-1. In addition, nocodazole negatively affected actin polymerization, and weakly activated ERK and p38α but significantly activated JNK in non-infected cells. After subsequent infection, nocodazole weakly inhibited activation of ERK and p38α. For the in vivo tests, nocodazole -treated mice displayed elevated levels of IFN-γ, MCP-1 and IL-10 while Brucella-infected nocodazole -treated mice showed high levels of TNF, IFN-γ, MCP-1, IL-10 and IL-6 as compared to controls. Furthermore, nocodazole treatment reduced inflammation and Brucella proliferation in the spleens of mice. These findings highlight the potential use of nocodazole for the control of brucellosis although further investigations are encouraged to validate its therapeutic use in animal hosts.

Publication Type
Journal
Publication Sub Type
Journal Article, Original
Title
Microbial Pathogenesis
Frequency
Monthly
Publication Date
February 2017
Volume
103
Issue
Notplicable
Page(s)
87–93
LocationLocation CodeAvailable FormatAvailability
Science Direct Website Fulltext External Link (View)

Copyright © One Window Project 2018. All rights reserved.