Differential expression of TLRs 2, 4, 9, iNOS and TNF-α and arginase activity in peripheral blood monocytes from glucantime unresponsive and responsive patients with anthroponotic cutaneous leishmaniasis caused by Leishmania tropica.


Journal

Microbial pathogenesis
ISSN: 1096-1208
Titre abrégé: Microb Pathog
Pays: England
ID NLM: 8606191

Informations de publication

Date de publication:
Jan 2019
Historique:
received: 31 08 2018
revised: 29 10 2018
accepted: 02 11 2018
pubmed: 7 11 2018
medline: 5 3 2019
entrez: 7 11 2018
Statut: ppublish

Résumé

Detection of the mechanism of host/parasite interactions in unresponsive forms of anthroponotic cutaneous leishmaniasis (ACL) caused by Leishmania tropica is helpful for immunotherapy and vaccine development. In the present study, the gene expression of toll-like receptors (TLRs), TNF-α, iNOS and also arginase (ARG) activity in monocytes from Glucantime unresponsive in comparison to responsive patients infected with L. tropica was investigated. In this case-control study, patients with unresponsive (n = 10) and responsive (n = 10) ACL were recruited. Gene expression of TLR2, TLR4, TLR9, TNF-α and iNOS was analyzed in L. tropica-exposed monocytes. The level of ARG activity in both isolated promastigotes and the lysates of monocytes was also determined. L. tropica-exposed monocytes represented higher expression of all three TLRs and TNF-α and lower expression of iNOS compared to unexposed ones in both groups of patients. Results revealed a significant down-regulation of TLR2 and TNF-α and up-regulation of TLR9 expression in unresponsive isolates in comparison to responsive ones. Besides, ARG level showed a significant increase in L. tropica-stimulated monocytes and cultured promastigotes from unresponsive isolates versus responsive ones. The decreased TLR2, TLR4, TNF-α and iNOS and the increased level of TLR9 expression in L. tropica-exposed monocytes from unresponsive isolates and also the increment in ARG activity in their promastigotes and monocytes, might possibly be involved in the severity of the disease and leading to Glucantime unresponsiveness.

Sections du résumé

BACKGROUND BACKGROUND
Detection of the mechanism of host/parasite interactions in unresponsive forms of anthroponotic cutaneous leishmaniasis (ACL) caused by Leishmania tropica is helpful for immunotherapy and vaccine development. In the present study, the gene expression of toll-like receptors (TLRs), TNF-α, iNOS and also arginase (ARG) activity in monocytes from Glucantime unresponsive in comparison to responsive patients infected with L. tropica was investigated.
METHODS METHODS
In this case-control study, patients with unresponsive (n = 10) and responsive (n = 10) ACL were recruited. Gene expression of TLR2, TLR4, TLR9, TNF-α and iNOS was analyzed in L. tropica-exposed monocytes. The level of ARG activity in both isolated promastigotes and the lysates of monocytes was also determined.
RESULTS RESULTS
L. tropica-exposed monocytes represented higher expression of all three TLRs and TNF-α and lower expression of iNOS compared to unexposed ones in both groups of patients. Results revealed a significant down-regulation of TLR2 and TNF-α and up-regulation of TLR9 expression in unresponsive isolates in comparison to responsive ones. Besides, ARG level showed a significant increase in L. tropica-stimulated monocytes and cultured promastigotes from unresponsive isolates versus responsive ones.
CONCLUSIONS CONCLUSIONS
The decreased TLR2, TLR4, TNF-α and iNOS and the increased level of TLR9 expression in L. tropica-exposed monocytes from unresponsive isolates and also the increment in ARG activity in their promastigotes and monocytes, might possibly be involved in the severity of the disease and leading to Glucantime unresponsiveness.

Identifiants

pubmed: 30399441
pii: S0882-4010(18)31510-9
doi: 10.1016/j.micpath.2018.11.004
pii:
doi:

Substances chimiques

TLR10 protein, human 0
TLR2 protein, human 0
TLR4 protein, human 0
Toll-Like Receptor 10 0
Toll-Like Receptor 2 0
Toll-Like Receptor 4 0
Toll-Like Receptors 0
Tumor Necrosis Factor-alpha 0
Meglumine Antimoniate 75G4TW236W
NOS2 protein, human EC 1.14.13.39
Nitric Oxide Synthase Type II EC 1.14.13.39
Arginase EC 3.5.3.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

368-378

Informations de copyright

Copyright © 2018 Elsevier Ltd. All rights reserved.

Auteurs

Razieh Tavakoli Oliaee (RT)

Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran.

Iraj Sharifi (I)

Leishmaniasis Research Center, Kerman University of Medical Sciences, Kerman, Iran. Electronic address: iraj.sharifi@yahoo.com.

Ali Afgar (A)

Research Center for Hydatid Disease in Iran, Kerman University of Medical Sciences, Kerman, Iran.

Abdollah Jafarzadeh (A)

Department of Immunology, Medical School, Kerman University of Medical Sciences, Kerman, Iran.

Amir Tavakoli Kareshk (AT)

Infectious Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran.

Mehdi Bamorovat (M)

Leishmaniasis Research Center, Kerman University of Medical Sciences, Kerman, Iran.

Hamid Sharifi (H)

HIV/STI Surveillance Research Center, WHO Collaborating Center for HIV Surveillance, Institute for Futures Studies in Health, Kerman University of Medical Sciences, Kerman, Iran.

Zahra Babaei (Z)

Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran; Leishmaniasis Research Center, Kerman University of Medical Sciences, Kerman, Iran.

Amir Keyhani (A)

Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran.

Alireza Keyhani (A)

Leishmaniasis Research Center, Kerman University of Medical Sciences, Kerman, Iran.

Leili Abedi (L)

Department of Statistics and Epidemiology, Faculty of Health, Kerman University of Medical Sciences, Kerman, Iran.

Fatemeh Sharifi (F)

Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.

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Classifications MeSH