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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.

Researchers

NameRole
1Suk Kim Author
2Hong Hee  Chang Author
3Hu Jang  Lee Author
4Wongi Min Author
5Tran Xuan Ngoc  Huy Author
6Lauren T. Arayan Author
7Huynh Tan  Hop Author
8Alisha Wehdnesday  B. Reyes Author

Related Institutions

Institutions NameRole
Institute of Animal Medicine,College of Veterinary Medicine - Gyeongsang National University Authors Affiliation
Department of Veterinary Paraclinical Sciences,College of Veterinary Medicine - University of the Philippines-Los Banos Authors Affiliation
Institute of Agriculture and Life Sciences - Gyeongsang National University Authors Affiliation

Publication Information

1.
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
Publisher:
Elsevier Ltd.

Abstract

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.


Physical Location

LocationCall NumberAvailable FormatAvailability
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