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: | Tran Xuan Ngoc Huy, Alisha Wehdnesday Bernardo Reyes, John Hwa Lee, Chang Keun Kang, Suk Kim, Wongi Min, Hu Jang Lee, Son Hai Vu, Lauren Togonon Arayan |
---|---|
Rok vydání: | 2019 |
Předmět: |
Benzylamines
Receptors CXCR4 Cell Survival media_common.quotation_subject medicine.medical_treatment Brucella abortus Brucella Cyclams Models Biological Microbiology Brucellosis Nitric oxide Mice 03 medical and health sciences chemistry.chemical_compound Chemokine receptor Heterocyclic Compounds medicine Animals Internalization 030304 developmental biology media_common Mice Inbred BALB C 0303 health sciences CXCR4 antagonist General Veterinary biology 030306 microbiology Kinase General Medicine biology.organism_classification Specific Pathogen-Free Organisms RAW 264.7 Cells Cytokine chemistry Female Tumor necrosis factor alpha Disease Susceptibility |
Zdroj: | Veterinary Microbiology. 237:108402 |
ISSN: | 0378-1135 |
Popis: | 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. |
Databáze: | OpenAIRE |
Externí odkaz: |