The Serum Level of CXCL9, CXCL10, and CXCL11 and the Expression of CXCR3 of Peripheral Blood Mononuclear Cells in Brucellosis Patients.
Journal
Current microbiology
ISSN: 1432-0991
Titre abrégé: Curr Microbiol
Pays: United States
ID NLM: 7808448
Informations de publication
Date de publication:
04 May 2023
04 May 2023
Historique:
received:
13
04
2022
accepted:
14
02
2023
medline:
8
5
2023
pubmed:
4
5
2023
entrez:
4
5
2023
Statut:
epublish
Résumé
Brucella spp. can replicate in human endothelial cells, inducing an inflammatory response with increased expression of chemokines. Although Brucella infects humans, its ability to induce the production of chemokines by lung cells is unknown. Therefore, the current investigation was designed to examine the association between brucellosis and CXCL9, 10, and 11 chemokines. The patient group included 71 patients suffering from Brucella infection and the control group consisted of 50 healthy ranchers from the same geographical area. Serum levels of CXCL9, CXCL10, and CXCL11 were analyzed by ELISA. The fold changes of CXCR3 expression against β-actin were determined by real-time-PCR technique. Western blotting analysis was also applied for evaluating the expression of CXCR3 at protein level. The results of this study showed that the serum levels of CXCL9, CXCL10, and CXCL11 are significantly increased in acute brucellosis patients in comparison to control as indicated by ELISA test, mRNA levels of CXCR3 by Real-time PCR as well as protein levels of CXCR3 by Western blot analysis. According to findings, these chemokines have the potential to serve as markers for brucellosis patients. Taken together, cytokine/chemokine network was active in acute brucellosis patients, and it is suggested to evaluate other cytokines in future studies.
Identifiants
pubmed: 37140634
doi: 10.1007/s00284-023-03230-2
pii: 10.1007/s00284-023-03230-2
doi:
Substances chimiques
Chemokine CXCL10
0
CXCL9 protein, human
0
Chemokine CXCL9
0
CXCL10 protein, human
0
CXCL11 protein, human
0
Chemokine CXCL11
0
CXCR3 protein, human
0
Receptors, CXCR3
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
201Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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