scholarly journals Infection with Toxoplasma gondii Increases Atherosclerotic Lesion in ApoE-Deficient Mice

2004 ◽  
Vol 72 (6) ◽  
pp. 3571-3576 ◽  
Author(s):  
Luciane R. Portugal ◽  
Luciana R. Fernandes ◽  
Giovana C. Cesar ◽  
Helton C. Santiago ◽  
Dirce R. Oliveira ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Atherosclerotic Lesion ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Lesion Size ◽  
Liver Cholesterol ◽  
Proinflammatory Response ◽  
Aortic Lesion ◽  
Monocyte Chemoattractant Protein 1 ◽  
Ifn Γ

ABSTRACT Toxoplasma gondii is an intracellular protozoan that elicits a potent inflammatory response during the acute phase of infection. Herein, we evaluate whether T. gondii infection alters the natural course of aortic lesions. ApoE knockout mice were infected with T. gondii, and at 5 weeks of infection, serum, feces, and liver cholesterol; aortic lesion size, cellularity, and inflammatory cytokines; and levels of serum nitrite and gamma interferon (IFN-γ) were analyzed. Our results showed that serum cholesterol and atherogenic lipoproteins were reduced after T. gondii infection. The reduction of serum levels of total cholesterol and atherogenic lipoproteins was associated with increases in the aortic lesion area, numbers of inflammatory cells, and expression of monocyte chemoattractant protein 1 and inducible nitric oxide synthase mRNA in the site of lesions as well as elevated concentrations of IFN-γ and nitrite in sera of T. gondii-infected animals. These results suggest that infection with T. gondii accelerates atherosclerotic development by stimulating the proinflammatory response and oxidative stress, thereby increasing the area of aortic lesion.

scholarly journals CCR7-Dependent Immunity during Acute Toxoplasma gondii Infection

2010 ◽  
Vol 78 (5) ◽  
pp. 2257-2263 ◽  
Author(s):  
Shahani Noor ◽  
Andrew S. Habashy ◽  
J. Philip Nance ◽  
Robin T. Clark ◽  
Kiav Nemati ◽  
...  
Keyword(s):  
T Cell ◽  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Parasite Burden ◽  
Serum Levels ◽  
Interleukin 12 ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Absolute Requirement ◽  
Ifn Γ

ABSTRACT The chemokine receptor CCR7 is a well-established homing receptor for dendritic cells and T cells. Interactions with its ligands, CCL19 and CCL21, facilitate priming of immune responses in lymphoid tissue, yet CCR7-independent immune responses can be generated in the presence of sufficient antigen. In these studies, we investigated the role of CCR7 signaling in the generation of protective immune responses to the intracellular protozoan parasite Toxoplasma gondii. The results demonstrated a significant increase in the expression of CCL19, CCL21, and CCR7 in peripheral and central nervous system (CNS) tissues over the course of infection. Unexpectedly, despite the presence of abundant antigen, CCR7 was an absolute requirement for protective immunity to T. gondii, as CCR7−/− mice succumbed to the parasite early in the acute phase of infection. Although serum levels of interleukin 12 (IL-12), IL-6, tumor necrosis factor alpha (TNF-α), and IL-10 remained unchanged, there was a significant decrease in CCL2/monocyte chemoattractant protein 1 (MCP-1) and inflammatory monocyte recruitment to the site of infection. In addition, CCR7−/− mice failed to produce sufficient gamma interferon (IFN-γ), a critical Th1-associated effector cytokine required to control parasite replication. As a result, there was increased parasite dissemination and a significant increase in parasite burden in the lungs, livers, and brains of infected mice. Adoptive-transfer experiments revealed that expression of CCR7 on the T-cell compartment alone is sufficient to enable T-cell priming, increase IFN-γ production, and allow the survival of CCR7−/− mice. These data demonstrate an absolute requirement for T-cell expression of CCR7 for the generation of protective immune responses to Toxoplasma infection.

scholarly journals Monocyte chemoattractant protein-1 involvement in the α-tocopherol-induced reduction of atherosclerotic lesions in apolipoprotein E knockout mice

2003 ◽  
Vol 90 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Maria C. G. Peluzio ◽  
Emir Miguel ◽  
Thaís C. Drumond ◽  
Giovana C. César ◽  
Helton C. Santiago ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Knockout Mice ◽  
Quantitative Polymerase Chain Reaction ◽  
Lesion Size ◽  
Tocopheryl Acetate ◽  
Aortic Lesion ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Apolipoprotein E Knockout Mice

We studied the effects of α-tocopheryl acetate supplementation on the development of fatty streaks and its ability to modulate the expression of monocyte chemoattractant protein (MCP)-1 in aortic lesions of apoliprotein E knockout mice. For this purpose, 16-week-old apolipoprotein E knockout mice received α-tocopherol supplemention ((800 mg)/kg diet) for 6 weeks. After this time, total and lipoprotein cholesterol in the serum, hepatic tocopherol, aortic lesion area and MCP-1 (protein and mRNA) expression were analysed. Our present results showed that the dietary supplementation with α-tocopherol did not reduce serum cholesterol nor change lipoprotein profile, but it reduced the area of the aortic lesion by 55%. The reduction in the lesion size was correlated with the reduced expression of MCP-1 mRNA and protein, as detected by real-time quantitative polymerase chain reaction and immunohistochemistry respectively. In conclusion, the results obtained here are relevant to the study of atherosclerosis, as they correlate the effectiveness of vitamin E supplementation in inhibiting the plaque formation with diminished expression of MCP-1 at the aortic lesion.

scholarly journals Evaluation of Immunogenic Effect of Toxoplasma gondii RecombinantSAG-1 Antigen with Propranolol as Adjuvant in BALB/c Mice

2019 ◽  
Vol 9 (4) ◽  
pp. 632-639
Author(s):  
Esmaeil Abasi ◽  
Shahram Shahabi ◽  
Majid Golkar ◽  
Peyman Khezri ◽  
Habib Mohammadzadeh Hajipirloo
Keyword(s):  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Lymphocyte Proliferation ◽  
Challenge Test ◽  
Optimal Dose ◽  
Serum Levels ◽  
Control Group ◽  
Interleukin 5 ◽  
Ifn Γ ◽  
Positive Effect

Purpose: Propranolol as a novel adjuvant, was used to evaluate the immunogenic effect of threedoses of recombinant SAG-1 (rSAG-1) antigen of Toxoplasma gondii in BALB/c mice for findingthe optimal dose, and was compared with efficacy of tachyzoite lysate antigen (TLA).Methods: Eight different groups of 15 BALB/c mice received different volumes of theimmunogenic material (three doses of r SAG-1 and one dose of TLA antigens), with or withoutpropranolol adjuvant, subcutaneously. The control group mice received only PBS. Three weeksafter the last immunization, the serum levels of IgG2a, IgG1 and IgG total antibodies againstTLA, splenic interleukin-5 (IL-5) and Interferon-gamma (IFN-γ) (produced against TLA) and thesplenic lymphocyte proliferation after adding TLA were measured to evaluate humoral andcellular immune responses. Challenge test was performed by subcutaneously injection of 1000alive and active tachyzoites in to five mice per each group and survival days for each group ofmice were recorded.Results: The mice group that received propranolol adjuvant and 20 μg of r SAG-1 antigenper dose of injection showed significantly more IFN-γ production, more proliferation ofsplenic lymphocytes and higher anti-TLA-specific IgG2a production (three main indexes forcell mediated immunity) in comparison with other groups. Moreover, in the challenge test,this group of mice had a significantly increased survival time, indicating the positive effect ofpropranolol in the more stimulating of cellular immunity that is necessary for toxoplasmosisprevention or suppress.Conclusion: Our results showed that T. gondii rSAG-1 antigen in combination with propranololas adjuvant (which can induce Th1 related responses) are good candidates for further study toa vaccine design.<br />

scholarly journals Immunobiotic and Paraprobiotic Potential Effect of Lactobacillus casei in a Systemic Toxoplasmosis Murine Model

2020 ◽  
Vol 8 (1) ◽  
pp. 113 ◽  
Author(s):  
Angel Gustavo Salas-Lais ◽  
Atzín Robles-Contreras ◽  
José Abraham Balderas-López ◽  
Victor Manuel Bautista-de Lucio
Keyword(s):  
Toxoplasma Gondii ◽  
Lactobacillus Casei ◽  
Peritoneal Macrophages ◽  
Potential Effect ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Parasitic Load ◽  
Ifn Γ ◽  
Necrosis Factor

One of the main characteristics of probiotics is their ability to stimulate and modulate the immune response regardless of their viability. Lactobacillus casei (Lc) can stimulate local and systemic immunity, in addition to the activation of macrophages at sites distant from the intestine. Activated macrophages limit the replication of intracellular protozoa, such as Toxoplasma gondii, through the production of nitric oxide. The present study aimed to evaluate the protection generated by treatment with viable and non-viable Lc in the murine systemic toxoplasmosis model. CD1 male mice were treated with viable Lc (immunobiotic) and non-viable Lc (paraprobiotic), infected with tachyzoites of Toxoplasma gondii RH strain. The reduction of the parasitic load, activation of peritoneal macrophages, inflammatory cytokines, and cell populations was evaluated at 7 days post-infection, in addition to the survival. The immunobiotic and paraprobiotic reduced the parasitic load, but only the immunobiotic increased the activation of peritoneal macrophages, and the production of interferon-gamma (IFN-γ), tumor necrosis factor (TNF), and interleukin-6 (IL-6) while the paraprobiotic increased the production of monocyte chemoattractant protein-1 (MCP-1) and T CD4+CD44+ lymphocytes. Viable and non-viable Lc increases survival but does not prevent the death of animals. The results provide evidence about the remote immunological stimulation of viable and non-viable Lc in an in vivo parasitic model.

P6194Therapeutic effect of nanoliposomal anti-PCSK9 vaccine on hypercholesterolemia and atherosclerosis in C57BL/6 mice

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A A Momtazi-Borojeni ◽  
M R Jaafari ◽  
M Banach ◽  
A Sahebkar
Keyword(s):  
Plasma Levels ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Density Lipoprotein ◽  
Lesion Size ◽  
Lipid Lowering ◽  
Therapeutic Effects ◽  
Igg Antibody ◽  
Ifn Γ

Abstract Background Proprotein convertase subtilisin/kexin 9 (PCSK9) promotes hypercholesterolemia through reducing protein level of liver low-density lipoprotein (LDL) receptor (LDLR). Currently, PCSK9 inhibition is known as an efficient lipid-lowering approach. Purpose Here, we constructed a liposomal anti-PCSK9 vaccine, and evaluated its therapeutic effects on dyslipidemia and atherosclerosis in atherosclerotic mice. Methods Liposomal anti-PCSK9 vaccine was prepared viaattaching immunogenic peptide, termed Immunogenic Fused PCSK9-Tetanus (IFPT), on the surface of nanoliposome carriers by using DSPE-PEG-Maleimide lipid (L-IFPT). The L-IFPT formulation was adsorbed to Alum adjuvant (L-IFPTA+) and administrated subcutaneously four times with a bi-weekly interval in hypercholesterolemic C57BL/6 mice. Plasma levels of anti-PCSK9 antibody, plasma concentration of PCSK9 protein, effect of anti-PCSK9 antibody on PCSK9-LDLR interaction, protein levels of liver LDLR, lipid profile, as well as atherosclerotic lesion size and severity were measured in the vaccinated hypercholesterolemic mice. To determine immune safety, Inflammatory response was measured by evaluating IFN-γ and IL-10 producing splenic cells using ELISpot assay. Results L-IFPTA+vaccine promoted the high IgG antibody response against PCSK9 peptide in the hypercholesterolemic mice. L-IFPTA+-induced antibodies targeted plasma PCSK9 and thereby decreased plasma consecration of PCSK9, which was associated with the reduced PCSK9-LDLR interaction and the increased liver levels of LDLR protein. Inhibitory effect of L-IFPTA+vaccine was accompanied with a significant reduction of plasma levels of total cholesterol (TC), LDL-C, and VLDL-C. Interestingly, L-IFPTA+vaccine could considerably reduce atherosclerotic lesion size and intima to media thicknessin hypercholesterolemic mice. Long-term evaluation of hypercholesterolemic vaccinated mice showed that L-IFPTA+vaccine was able to promote a long-lasting anti-PCSK9 antibody titration, which was paralleled by a significant reduction of LDL-C over 16 weeks post prime immunization (Figure). Splenocytes isolated from vaccinated mice indicated the reduced IFN-γ producing cells and the elevated IL-10 producing cells, suggesting immune safety of liposomal anti-PCSK9 vaccine. Figure 1 Conclusions L-IFPTA+vaccine induced efficient anti-PCSK9 antibodies which could exert long-term therapeutic effect on hypercholesterolemia and atherosclerosis in mice, revealing a feasible vaccine-based approach for managing hypercholesterolemia and cardiovascular disease.

Abstract 647: Induction of Cardiovascular Calcification in Non-transgenic Mice via a Single Injection of Pcsk9 Adeno-associated Viral Vector

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Claudia Goettsch ◽  
Joshua Hutcheson ◽  
Sumihiko Hagita ◽  
Maximillian Rogers ◽  
Jung Choi ◽  
...  
Keyword(s):  
Total Cholesterol ◽  
Near Infrared ◽  
Viral Vector ◽  
Low Density Lipoprotein ◽  
Atherosclerotic Lesion ◽  
Density Lipoprotein ◽  
Serum Levels ◽  
Lesion Size ◽  
Aortic Calcification

Background: Studying atherosclerotic calcification in vivo requires mouse models with genetic deletion of low-density lipoprotein receptor (Ldlr) or apolipoprotein E. A previous study showed a rapid induction of atherosclerosis by proprotein convertase subtilisin/kexin type 9 (PCSK9) in mice. Here, we hypothesize that this method is a useful in vivo tool to study cardiovascular calcification in non-genetically modified C57BL/6 mice. Results: 10 week old C57BL/6 mice received a single tail vein injection of recombinant adeno-associated viral vector (AAV) encoding PCSK9 (rAAV8/D377Y-mPCSK9). Ldlr -/- and saline injected C57BL/6 mice served as controls. Mice consumed a high-fat, high-cholesterol (HF/HC) diet for 15-20 weeks. PCSK9 and total cholesterol serum levels were significantly increased within one week after injection and maintained for 20 weeks (cholesterol: 82 mg/dL to 820 mg/dL, p<0.01; PCSK9: 0.14 μg/ml to 20 μg/ml, p<0.01). Total cholesterol levels remained 20-30% lower than those of of Ldlr -/- mice. Atherosclerotic lesion size was similar between PSCK9 and Ldlr -/- mice. Saline injected mice did not show any lesions. Plaque collagen content was 31.9%±6.6 in PCSK9 mice and 62.9%±16.6 in Ldlr -/- mice at 15 weeks of HF/HC diet (p=0.01). However, by 20 weeks, the PCSK9 mice had 57.9%±18.6 plaque collagen, suggesting a different stage of plaque progression. Fluorescence reflectance imaging of a near infrared calcium tracer in intact arteries detected 0.4%±0.4 aortic calcification in PCSK9 mice and 9.7%±1.6 in Ldlr -/- mice at 15 weeks of HF/HC diet (p=0.01); by 20 weeks, the PCSK9 mice had 5.3%±1.0 aortic calcification. Tissue non-specific alkaline phosphatase activity positive lesion area was 7.9%±4.0 and 8.3%±2.6 in PCSK9 mice and 10.8%±2.5 and 12.7%±1.7in Ldlr -/- mice at 15 and 20 weeks, respectively. Immunofluorescence analysis demonstrated accumulation of CD68 and RUNX2-positive cells in the plaques of PCSK9 mice similar to Ldlr -/- . Conclusion: While injection of recombinant AAV encoding PCSK9 into C57BL/6 mice induces atherosclerotic calcification with slower sclerotic plaque remodeling compared to Ldlr -/- mice, it may serve as a useful tool to study cardiovascular calcification in mice independent of their genetic background.

scholarly journals Pleiotropic Effects of the Protease-Activated Receptor 1 (PAR1) Inhibitor, Vorapaxar, on Atherosclerosis and Vascular Inflammation

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3517
Author(s):  
Julian Friebel ◽  
Eileen Moritz ◽  
Marco Witkowski ◽  
Kai Jakobs ◽  
Elisabeth Strässler ◽  
...  
Keyword(s):  
Vascular Inflammation ◽  
Atherosclerotic Lesion ◽  
Inflammatory Cells ◽  
Endothelial Activation ◽  
Lesion Size ◽  
Pleiotropic Effects ◽  
Knock Out ◽  
Cytokines And Chemokines ◽  
Protease Activated Receptor 1 ◽  
Vascular Adhesion

Background: Protease-activated receptor 1 (PAR1) and toll-like receptors (TLRs) are inflammatory mediators contributing to atherogenesis and atherothrombosis. Vorapaxar, which selectively antagonizes PAR1-signaling, is an approved, add-on antiplatelet therapy for secondary prevention. The non-hemostatic, platelet-independent, pleiotropic effects of vorapaxar have not yet been studied. Methods and Results: Cellular targets of PAR1 signaling in the vasculature were identified in three patient cohorts with atherosclerotic disease. Evaluation of plasma biomarkers (n = 190) and gene expression in endomyocardial biopsies (EMBs) (n = 12) revealed that PAR1 expression correlated with endothelial activation and vascular inflammation. PAR1 colocalized with TLR2/4 in human carotid plaques and was associated with TLR2/4 gene transcription in EMBs. In addition, vorapaxar reduced atherosclerotic lesion size in apolipoprotein E–knock out (ApoEko) mice. This reduction was associated with reduced expression of vascular adhesion molecules and TLR2/4 presence, both in isolated murine endothelial cells and the aorta. Thrombin-induced uptake of oxLDL was augmented by additional TLR2/4 stimulation and abrogated by vorapaxar. Plaque-infiltrating pro-inflammatory cells were reduced in vorapaxar-treated ApoEko mice. A shift toward M2 macrophages paralleled a decreased transcription of pro-inflammatory cytokines and chemokines. Conclusions: PAR1 inhibition with vorapaxar may be effective in reducing residual thrombo-inflammatory event risk in patients with atherosclerosis independent of its effect on platelets.

scholarly journals Toxoplasma gondii Upregulates Interleukin-12 To Prevent Plasmodium berghei-Induced Experimental Cerebral Malaria

2014 ◽  
Vol 82 (3) ◽  
pp. 1343-1353 ◽  
Author(s):  
Erik W. Settles ◽  
Lindsey A. Moser ◽  
Tajie H. Harris ◽  
Laura J. Knoll
Keyword(s):  
Toxoplasma Gondii ◽  
Cerebral Malaria ◽  
Plasmodium Berghei ◽  
Serum Levels ◽  
Interleukin 12 ◽  
Experimental Cerebral Malaria ◽  
Content Type ◽  
T Cell Infiltration ◽  
Ifn Γ ◽  
Deficient Mice

ABSTRACTA chronic infection with the parasiteToxoplasma gondiihas previously been shown to protect mice against subsequent viral, bacterial, or protozoal infections. Here we have shown that a chronicT. gondiiinfection can preventPlasmodium bergheiANKA-induced experimental cerebral malaria (ECM) in C57BL/6 mice. Treatment with solubleT. gondiiantigens (STAg) reduced parasite sequestration and T cell infiltration in the brains ofP. berghei-infected mice. Administration of STAg also preserved blood-brain barrier function, reduced ECM symptoms, and significantly decreased mortality. STAg treatment 24 h post-P. bergheiinfection led to a rapid increase in serum levels of interleukin 12 (IL-12) and gamma interferon (IFN-γ). By 5 days afterP. bergheiinfection, STAg-treated mice had reduced IFN-γ levels compared to those of mock-treated mice, suggesting that reductions in IFN-γ at the time of ECM onset protected against lethality. Using IL-10- and IL-12βR-deficient mice, we found that STAg-induced protection from ECM is IL-10 independent but IL-12 dependent. Treatment ofP. berghei-infected mice with recombinant IL-12 significantly decreased parasitemia and mortality. These data suggest that IL-12, either induced by STAg or injected as a recombinant protein, mediates protection from ECM-associated pathology potentially through early induction of IFN-γ and reduction in parasitemia. These results highlight the importance of early IL-12 induction in protection against ECM.

scholarly journals Dietary Antioxidants Decrease Serum Soluble Adhesion Molecule (sVCAM-1, sICAM-1) but not Chemokine (JE/MCP-1, KC) Concentrations, and Reduce Atherosclerosis in C57BL but Not ApoE*3 Leiden Mice Fed an Atherogenic Diet

2005 ◽  
Vol 21 (4) ◽  
pp. 181-190 ◽  
Author(s):  
Nuala Murphy ◽  
David C Grimsditch ◽  
Martin Vidgeon-Hart ◽  
Pieter H.E. Groot ◽  
Philip Overend ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Atherosclerotic Lesion ◽  
Transgenic Animals ◽  
Serum Levels ◽  
Lesion Size ◽  
Atherogenic Diet ◽  
Initial Increase ◽  
Dietary Antioxidants ◽  
Soluble Adhesion Molecules ◽  
Cellular Expression

Dietary antioxidants are reported to suppress cellular expression of chemokines and adhesion molecules that recruit monocytes to the artery wall during atherosclerosis. In the present study we measured the effect of feeding apoE*3 Leiden mice or their non-transgenic (C57BL) littermates with atherogenic diets either deficient in, or supplemented with, dietary antioxidants (vitamin E, vitamin C and β-carotene) for 12 weeks, on serum levels of CC (JE/MCP-1) and CXC (KC) chemokines and soluble adhesion molecules (sVCAM-1, sICAM-1) and atherosclerotic lesion size. ApoE*3 Leiden mice developed gross hypercholesterolaemia, and markedly accelerated (10–20 fold;P< 0.0001) atherogenesis, compared with non-transgenic animals. Antioxidant consumption reduced lesion area in non-transgenic, but not apoE*3 Leiden, mice. Serum sVCAM-1 and sICAM-1 levels were significantly (P< 0.0001) increased (sVCAM-1 up to 3.9 fold; sICAM-1 up to 2.4 fold) by 4—8 weeks in all groups, and then declined. The initial increase in the concentration of adhesion molecules was reduced by 38%— 61% (P< 0.05) by antioxidant consumption, particularly in non-transgenic mice. By contrast, serum chemokine levels tended to increase more rapidly from baseline in apoE*3 Leiden mice, compared with non-transgenic animals, but were unaffected by dietary antioxidants. We conclude that dietary antioxidants reduce circulating soluble adhesion molecules and atherosclerosis in C57BL mice.

IL-10-592 A/C Gene Polymorphism and Cytokine Levels are Associated with Susceptibility to Drug Resistance in Tuberculosis

2020 ◽  
Vol 8 (3) ◽  
pp. 103-112
Author(s):  
Atefeh SADEGHI SHERMEH ◽  
Majid KHOSHMIRSAFA ◽  
Ali-Akbar DELBANDI ◽  
Payam TABARSI ◽  
Esmaeil MORTAZ ◽  
...  
Keyword(s):  
Serum Levels ◽  
World Health ◽  
Control Group ◽  
Drug Resistant ◽  
Nucleotide Polymorphisms ◽  
Genotype Frequencies ◽  
Cytokine Levels ◽  
Ifn Γ ◽  
Health Organization ◽  
And Function

Introduction: Tuberculosis (TB) and especially resistant forms of it have a substantial economic burden on the community health system for diagnosis and treatment each year. Thus, investigation of this field is a priority for the world health organization (WHO). Cytokines play important roles in the relationship between the immune system and tuberculosis. Genetic variations especially single nucleotide polymorphisms (SNPs) impact cytokine levels and function against TB. Material and Methods: In this research SNPs in IFN-γ (+874 T/A) and IL-10 (-592 A/C) genes, and the effects of these SNPs on cytokine levels in a total of 87 tuberculosis patients and 100 healthy controls (HCs) were studied. TB patients divided into two groups: 1) 67 drug-sensitive (DS-TB) and 2) 20 drug-resistant (DR-TB) according to drug sensitivity test using polymerase chain reaction (PCR). For the genotyping of two SNPs, the PCR-based method was used and IFN-γ and IL-10 levels were measured by ELISA in pulmonary tuberculosis (PTB) and control group. Results: In -592A/C SNP, only two genotypes (AA, AC) were observed and both genotypes showed statistically significant differences between DR-TB and HCs (p=0.011). IL-10 serum levels in PTB patients were higher than HCs (p=0.02). The serum levels of IFN-γ were significantly higher in DS-TB patients than that of the other two groups (p<0.001); however, no significant differences were observed for allele and genotype frequencies in IFN-γ +874. Conclusions: Our results suggest that the SNP at -592 position of IL-10 gene may be associated with the susceptibility to DR-TB. However, further investigation is necessary. Keywords: Polymorphism, IFN-γ, IL-10, tuberculosis, drug-resistant tuberculosis

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