Chemokine receptor 4 (CXCR4) blockade enhances resistance to bacterial internalization in RAW264.7 cells and AMD3100, a CXCR4 antagonist, attenuates susceptibility to Brucella abortus 544 infection in a murine model.

Autor: Reyes AWB; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Arayan LT; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Huy TXN; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Vu SH; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Kang CK; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Min W; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Lee HJ; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Lee JH; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea., Kim S; Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea. Electronic address: kimsuk@gnu.ac.kr.
Jazyk: angličtina
Zdroj: Veterinary microbiology [Vet Microbiol] 2019 Oct; Vol. 237, pp. 108402. Date of Electronic Publication: 2019 Aug 28.
DOI: 10.1016/j.vetmic.2019.108402
Abstrakt: We investigated the involvement of chemokine receptor type 4 (CXCR4) signaling on the outcome of Brucella (B.) abortus 544 infection in murine macrophages and in a mouse model. CXCR4 manipulation were first evaluated for Brucella invasion and intracellular survival efficiency, mitogen-activated protein kinases (ERK1/2, JNK, p38α) activation and generation of nitric oxide (NO), and then in the splenic bacterial proliferation and cytokine production in BALB/c mice. CXCR4 blockade is involved in the successful control of Brucella invasion, reduction of ERK1/2 phosphorylation and inhibition of nitric oxide release from macrophages. Furthermore, using a reported CXCR4-specific antagonist AMD3100 resulted in splenomegaly but attenuated Brucella proliferation in these organs with elevated serum levels of MCP-1, TNF and IL-12. These findings provide insights on the contribution of CXCR4 signaling in the phagocytic pathway and immune modulation during B. abortus infection.
(Copyright © 2019 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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