Publications by authors named "Mohammad Vodjgani"

13 Publications

  • Page 1 of 1

Interpretation of Hematological, Biochemical, and Immunological Findings of COVID-19 Disease: Biomarkers Associated with Severity and Mortality.

Iran J Allergy Asthma Immunol 2021 Feb 11;20(1):46-66. Epub 2021 Feb 11.

Department of Biostatistics and Social Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.

The severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) spread rapidly all over the world in late 2019 and caused critical illness and death in some infected patients. This study aimed at examining several laboratory factors, especially inflammatory and immunological mediators, to identify severity and mortality associated biomarkers. Ninety-three hospitalized patients with confirmed coronavirus disease 2019 (COVID-19) were classified based on disease severity. The levels of biochemical, hematological, immunological, and inflammatory mediators were assessed, and their association with severity and mortality were evaluated. Hospitalized patients were mostly men (77.4%) with an average (standard deviation) age of 59.14 (14.81) years. The mortality rate was significantly higher in critical patients (85.7%). Increased serum levels of blood sugar, urea, creatinine, uric acid, phosphorus, total bilirubin, serum glutamic-oxaloacetic transaminase, serum glutamic-oxaloacetic transaminase, lactic dehydrogenase, C-reactive protein, ferritin, and procalcitonin were significantly prevalent (p=0.002, p<0.001, p<0.001, p=0.014, p=0.047, p=0.003, p<0.001, p<0.001, p<0.001, p<0.001, P<0.001, and p<0.001, respectively) in COVID-19 patients. Decreased red blood cell, hemoglobin, and hematocrit were significantly prevalent among COVID-19 patients than healthy control subjects (p<0.001 for all). Troponin-I, interleukin-6, neutrophil/lymphocyte ratio (NLR), procalcitonin, and D-dimer showed a significant association with the mortality of patients with specificity and sensitivity more than 60%. Age, sex, underlying diseases, blood oxygen pressure, complete blood count along with C-reactive protein, lactic dehydrogenase, procalcitonin, D-dimer, and interleukin-6 evaluation help to predict the severity and required management for COVID-19 patients. Further investigations are highly recommended in a larger cohort study for validation of the present findings.
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http://dx.doi.org/10.18502/ijaai.v20i1.5412DOI Listing
February 2021

Redox Imbalance in CD4+ T Cells of Relapsing-Remitting Multiple Sclerosis Patients.

Oxid Med Cell Longev 2020 2;2020:8860813. Epub 2020 Dec 2.

Immunology Department, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

As a prevalent autoimmune disease of the central nervous system in young adults, multiple sclerosis (MS) is mediated by T cells, particularly CD4+ subsets. Given the evidence that the perturbation in reactive oxygen species (ROS) production has a pivotal role in the onset and progression of MS, its regulation through the antioxidant molecules is too important. Here, we investigated the level of the redox system components in lymphocytes and CD4+ T cells of MS patients. The study was performed on relapsing-remitting MS (RRMS) patients ( = 29) and age- and sex-matched healthy controls ( = 15). Peripheral blood mononuclear cells (PBMCs) were cultured and stimulated by anti-CD3/CD28. The level of ROS, anion superoxide (O), and L-𝛾-glutamyl-Lcysteinylglycine (GSH) was measured by flow cytometry in lymphocytes/CD4+ T cells. The gene expression level of gp91phox, catalase, superoxide dismutase 1/2 (SOD), and nuclear factor-E2-related factor (Nrf2) was also measured by real-time PCR. We found that lymphocytes/CD4+ T cells of RRMS patients at the relapse phase significantly produced higher levels of ROS and O compared to patients at the remission phase ( value < 0.001) and healthy controls ( value < 0.001 and value < 0.05, respectively). Interestingly, the gene expression level of gp91phox, known as the catalytic subunit of the NADPH oxidase, significantly increased in MS patients at the relapse phase ( value < 0.05). Furthermore, the catalase expression augmented in patients at the acute phase ( value < 0.05), while an increased expression of SOD1 and Nrf2 was found in RRMS patients at relapse and remission phases ( value < 0.05). The increased production of ROS in CD4+ T cells of RRMS patients highlights the importance of amplifying antioxidant components as an efficient approach to ameliorate disease activity in MS patients.
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http://dx.doi.org/10.1155/2020/8860813DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7735833PMC
December 2020

The Influence of Reactive Oxygen Species in the Immune System and Pathogenesis of Multiple Sclerosis.

Autoimmune Dis 2020 25;2020:5793817. Epub 2020 Jun 25.

Immunology Department, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Multiple roles have been indicated for reactive oxygen species (ROS) in the immune system in recent years. ROS have been extensively studied due to their ability to damage DNA and other subcellular structures. Noticeably, they have been identified as a pivotal second messenger for T-cell receptor signaling and T-cell activation and participate in antigen cross-presentation and chemotaxis. As an agent with direct toxic effects on cells, ROS lead to the initiation of the autoimmune response. Moreover, ROS levels are regulated by antioxidant systems, which include enzymatic and nonenzymatic antioxidants. Enzymatic antioxidants include superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. Nonenzymatic antioxidants contain vitamins C, A, and E, glutathione, and thioredoxin. Particularly, cellular antioxidant systems have important functions in maintaining the redox system homeostasis. This review will discuss the significant roles of ROS generation and antioxidant systems under normal conditions, in the immune system, and pathogenesis of multiple sclerosis.
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http://dx.doi.org/10.1155/2020/5793817DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334772PMC
June 2020

Evaluation of ITGB2 (CD18) and SELL (CD62L) genes expression and methylation of ITGB2 promoter region in patients with systemic sclerosis.

Rheumatol Int 2018 Mar 22;38(3):489-498. Epub 2018 Jan 22.

Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran.

Systemic sclerosis (SSc), an autoimmune disease of connective tissue, is characterized by inflammation, fibrosis, and vessel endothelial damage. Products of Integrin subunit beta 2 (ITGB2) and selectin L (SELL) genes participate in several functional pathways of immune system. The aim of this investigation was to survey the transcript level of ITGB2 and SELL genes as well as methylation status of CpG sites in promoter region of differently expressed gene in PBMCs of SSc patients. PBMCs were isolated from whole blood of 50 SSc patients and 30 healthy controls. Total RNA and DNA contents of PBMCs were extracted. Gene expression was analyzed by real-time PCR using the SYBR Green PCR Master Mix. To investigate the methylation status of CpG sites, DNA samples were treated by bisulfite, amplified through nested PCR, and sequenced through Sanger difficult sequencing method. ITGB2 gene in PBMCs of SSc patients was overexpressed significantly in comparison to healthy controls. However, no altered SELL expression was observed. Three CpG sites of 12, 13 and 14 were significantly hypomethylated in patients group, despite overall methylation status of ITGB2 gene promoter revealed no significant difference between study groups. There was no statistically significant correlation between methylation status of ITGB2 promoter and the gene expression in patients. Regarding to lack of correlation of increased expression of ITGB2 with its promoter hypomethylation in SSc patients, our study suggests that upregulation of ITGB2 in PBMCs from SSc patients is probably due to another mechanism other than methylation alteration.
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http://dx.doi.org/10.1007/s00296-017-3915-yDOI Listing
March 2018

IRF7 gene expression profile and methylation of its promoter region in patients with systemic sclerosis.

Int J Rheum Dis 2017 Oct 26;20(10):1551-1561. Epub 2017 Sep 26.

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Objective: The aim of the current study was to evaluate if methylation status of CpG sites of interferon regulatory factor 7 (IRF7) promoter in peripheral blood mononuclear cells (PBMCs) of systemic sclerosis (SSc) patients is involved in pathogenesis of the disease.

Methods: PBMCs were isolated from whole blood of 50 SSc patients and 30 controls. After the extraction of total RNA and DNA contents from PBMCs, complementary DNA (cDNA) was synthesized. Afterwards, quantitative analysis of IRF7 messenger RNA (mRNA) was conducted by real-time polymerase chain reaction (PCR). To evaluate the methylation status of the promoter region of IRF7 gene, PCR products of bisulfite-treated DNA from SSc patients and controls were sequenced.

Results: The mRNA expression of IRF7 in PBMCs from patients compared with controls was significantly upregulated. While limited cutaneous SSc patients expressed the mRNA of IRF7 higher than controls, the diffuse cutaneous SSc group did not demonstrate significantly increased expression in comparison to controls. Insignificant promoter hypomethylation of IRF7 was observed in SSc patients compared with the control group. However, CpG2 hypomethylation was significantly associated with increased SSc risk. Furthermore, overall promoter methylation and mRNA level of IRF7 were significantly correlated with each other. Nonetheless, none of them correlated with Rodnan score of SSc patients. There was significant difference in IRF7 mRNA expression between CpG8 methylated and unmethylated SSc patients. Moreover, the difference of methylation and expression was not significant between anti-nuclear antibody (ANA)-positive and ANA-negative SSc patients.

Conclusions: It is suggested that hypomethylation of the IRF7 promoter might play a role in SSc pathogenesis, probably through promoting the IRF7 expression in PBMCs of patients with SSc.
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http://dx.doi.org/10.1111/1756-185X.13175DOI Listing
October 2017

Investigating the Effect of rs3783605 Single-nucleotide Polymorphism on the Activity of VCAM-1 Promoter in Human Umbilical Vein Endohelial Cells.

Iran J Allergy Asthma Immunol 2015 Apr;14(2):179-87

Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

The interaction between immune cells and endothelial lining of blood vessels is vital in many processes such as inflammatory and immune responses as well as cancer cell metastasis. The expression level of VCAM-1 is regulated by many factors including the promoter activity that is possibly affected by the single nucleotide polymorphisms (SNPs) present in the promoter. There are previous reports suggesting an important role for rs3783605 at -420 position in the pathogenesis of VCAM1-associated diseases. This is possibly due to the effect of this SNP on promoter activity and gene expression. Therefore, present study was designed to investigate the effect of rs3783605 on the activity of VCAM-1 gene promoter in human umbilical vein endothelial cells (HUVEC). In this study, two appropriate expression vectors containing VCAM1 promoter with different alleles of rs3783605 were constructed to express the Green Fluorescent Protein (GFP). Expression vectors were transfected into HUVECs and their EGFP expression level was assessed by the fluorescent microscopy and real-time PCR. Bright green fluorescence was seen in the HUVECs transfected by expression vector containing CMV promoter. The expression level in the cells transfected by vector containing promoter with A allele of rs3783605 was 0.14888 folds and G allele was about 0.37851 folds of cells transfected by vector having CMV promoter (p<0.001). Moreover, HUVECs transfected by G allele of rs3783605 showed about 2-fold higher transcriptional activity compared with the A allele, (p=0.049). Our findings showed that rs3783605 polymorphism may play a role in VCAM-1 gene expression. Therefore, it is likely that it may have an important role in the pathogenesis of VCAM1-associated diseases and tumor metastases.
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April 2015

Post challenging serum cytokine profile (Th1 & Th2) in the vaccinated mice (Balb/C) with a new formulation of Leishmania major antigen.

Turkiye Parazitol Derg 2013 ;37(4):233-40

Department of Immununology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran.

Objective: The aim of this study was to carry out experiments further to our previous new formulation to modify the Leishmania major antigen that had satisfactory results previously.

Methods: In this study we made a preliminary, new vaccine with the same methodology and selected two injection doses (100&200 μg/o.1 mL), three injection Groups: Leishmania plus BCG (LB), Leishmania plus new adjuvant (Teucrium Polium) [LT], Leishmania plus BCG and Teucrium Polium (LBT), and one susceptible mouse Group (Balb/c) and measure two types of cytokines: Th1 (IFN-γ, IL-12) and Th2 (IL-4, IL-10) We prepared crude antigen combinations by five different methods using antigens from L. major parasites. Phase I was done in the animal model. In our study, Leishmania antigen was examined both with BCG and the new adjuvant (TP) in three Groups in two injection doses (100.200 μg/1 mL) and Balb/c mice.

Results: Our results showed that in three injection Groups (LB, LT and LBT) that received each or both BCG and TP as adjutant with injection doses of 100 and 200 μg/1 mL with two booster doses: the LBT Group had the lowest IFNγ and highest IL-12 value, LT and LB Groups have equal IL-12, but LB have more IFNγ and IL-10 but less than IL-4 in the LT Group.

Conclusion: In this study, the LBT Group has statistical differences regarding IL-12 and IL-10 from the other Groups.
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http://dx.doi.org/10.5152/tpd.2013.2988DOI Listing
August 2014

Increased expression of CD69 antigen on human peripheral blood natural killer cells in patients with allergic rhinitis.

Iran J Allergy Asthma Immunol 2013 Mar;12(1):68-74

Department of Immunology, Mofid Children Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Allergic rhinitis (AR) is an inflammatory disorder of the nasal mucosa with high morbidity and prevalence. Natural killer (NK) cells might have a role in AR. We aimed to evaluate the changes of the markers and receptors on NK cells in AR patients compared to the non-atopic controls.Flow cytometric analysis was used with double staining of the Peripheral Blood Mononuclear Cells (PBMCs) to examine the expression of CD25 and CD69 markers, and NKG2D and NKG2A receptors on NK cells of 20 patients with AR and 20 non-atopic controls. The serum total IgE level was measured by Enzyme-linked Immunosorbent Assay.The expression of CD69 antigen on NK cells in AR patients was significantly higher than that of healthy group (p=0.03). No significant changes were observed between CD25, NKG2D and NKG2A expression on the surface of NK cells from healthy and AR subjects. Our study also showed that there was no significant correlation between the expression of CD69, CD25, NKG2D and NKG2A and level of serum total IgE in AR patients and normal subjects.These results indicated that the expression of CD69 antigen on NK cells of AR patients was increased. The high expression of CD69 on NK cells in AR patients suggested that these cells were activated, probably due to the cytokines secreted from allergen-stimulated T cells and activated monocytes.
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http://dx.doi.org/012.01/ijaai.688874DOI Listing
March 2013

Natural killer cells in allergic rhinitis patients and nonatopic controls.

Int Arch Allergy Immunol 2010 18;153(3):234-8. Epub 2010 May 18.

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Background: Allergic rhinitis (AR) is currently considered to be a worldwide problem. The role of type 2 cytokines in this disease has been established, and natural killer (NK) cells are possibly the source of cytokine secretions. This study was performed to confirm the existence of type 2 cytokine-secreting NK cells in AR patients and to determine their characteristics.

Methods: Twenty AR patients and 20 healthy nonatopic controls were included. Peripheral blood mononuclear cells were separated from heparinized blood by density gradient centrifugation. NK cells were enriched and cultured for 72 h. Cytokine secretion was measured by ELISA, and cytotoxicity assay was carried out using the PKH2-labeled K562 cell line. Intracytoplasmic cytokine staining and an analysis of surface markers of NK cells were performed on freshly isolated peripheral blood mononuclear cells using flow cytometry.

Results: Patients with AR had a higher percentage of NK cells compared to nonatopic subjects. The mean percentage of IL-4+ NK cells was significantly higher and that of IFN-γ+ NK cells was nonsignificantly lower in AR patients compared to healthy nonatopic controls. IL-13 secretion was also significantly higher in AR patients compared to nonatopic controls. While there was no difference between the case and the control groups with regard to the surface expression of CD40, CD45RO, and CD95, the expression of CD178 was significantly higher in the cases when compared to the controls. NK cell cytotoxicity was also significantly higher in AR patients compared to healthy controls.

Conclusions: This study confirms the existence of type 2 cytokine-secreting NK cells in AR and shows their increased number and enhanced cytotoxicity compared to normal individuals.
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http://dx.doi.org/10.1159/000314363DOI Listing
November 2010

Increased expression of TRAIL and its receptors on peripheral T-cells in type 1 diabetic patients.

Iran J Immunol 2007 Dec;4(4):197-205

Department of Immunology, Tehran University of Medical Sciences, Tehran, Iran.

Background: Type-I diabetes is an autoimmune inflammatory disease in which pancreatic beta-cells are selectively destroyed by infiltrating cells. TNF-related apoptosis-inducing ligand (TRAIL) is a type-II membrane protein of the TNF superfamily which is expressed in different tissues, including pancreas and lymphocytes. In humans, TRAIL interacts with four membrane receptors. TRAIL-R1 and TRAIL-R2 have cytoplasmic death domains, and can activate both caspases and NFkappaB pathways. The other two receptors, TRAIL-R3 and TRAIL-R4, are decoy receptors not capable of activating caspase cascade but may activate NF-kappaB and block apoptosis. As human beta cells are sensitive to TRAIL induced apoptosis, signaling via these molecules is considered to be a probable way of beta cell destruction. These molecules also are important in suppression of autorective T cells and immunoregulation.

Objective: To explore the importance of TRAIL and its receptors at pathogenesis of type-I diabetes, we compared expression of these molecules on T-cells of diabetic patients and healthy controls.

Methods: In this study, expression of TRAIL and its receptors at protein and mRNA levels were studied in freshly isolated peripheral T cells of 55 type I diabetic patients and 50 healthy individuals by flowcytometry, western blot and RT-PCR.

Results: We found that expression of TRAIL and its receptors in peripheral T-cells at both protein and mRNA levels are significantly increased in patients (except for TRAIL-R2 mRNA which was slightly higher in controls) but increase in TRAIL, TRAIL-R3 (2.7% vs. >0.5%) and TRAIL-R4 (2.6% vs. >0.5%) is more considerable. sTRAIL in sera of patients was significantly lower than in controls (P=0.01).

Conclusion: Our results explain resistance of autoreactive T-cells to immunoregulatory mechanisms. Besides, increased expression of TRAIL in autoreactive T-cells may play an important role in beta-cell destruction. Lower level of sTRAIL in diabetic patients may be a reason for hyperactivation of autoreactive T-cells.
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http://dx.doi.org/IJIv4i4A2DOI Listing
December 2007

Serum cytokines profiles in Iranian patients with preeclampsia.

Iran J Immunol 2007 Sep;4(3):179-85

Department of Immunology, School of Medicine, Medical Sciences, University of Tehran, Tehran, Iran.

Background: Preeclampsia is a major cause of mortality and morbidity and is also a leading cause of preterm birth and intrauterine growth retardation. Several studies have reported abnormal levels of cytokines in women with preeclampsia.

Objectives: To detect serum levels of various cytokines in pregnant women with and without preeclampsia in the third trimester of pregnancy.

Methods: Thirty patients with preeclampsia and thirty normal pregnant women were enrolled in the study. Blood samples were taken and serum levels of IFN gamma, IL-12p70, IL-18, IL-15, IL-4 and IL-10 were measured by enzyme-linked immunosorbent assay (ELISA).

Results: Preeclamptic women had significantly increased levels of circulating IL-12p70 (p < 0.05), IL-18 (p < 0.001), IL-4 (p < 0.001), IL-15 (p < 0.05) and IFN gamma (p < 0.001). By contrast, circulating levels of IL-10 were not significantly different between the two groups.

Conclusions: The present study supports the hypothesis of altered immune response in preeclampsia and suggests that dysregulation of cytokine expression occurs in preeclampsia with increased levels of IFN gamma, IL-12p70, IL-15, IL-18 and IL-4.
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http://dx.doi.org/IJIv4i3A7DOI Listing
September 2007

Decreased T cell response to mitogen and increased anti-cytoplasmic antibody in drug-free schizophrenic patients.

Iran J Immunol 2007 Mar;4(1):32-7

Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Background: Apart from genetic and environmental factors, activation of autoreactive mechanisms has been proposed to play a role in the pathogenesis of schizophrenia. In recent years, considerable work has been carried out to understand the role and contribution of the immune system in this disease.

Objective: To investigate the T cell response to phytohaemagglutinin (PHA) and determine the serum levels of anti-nuclear antibody (ANA), anti-cytoplasmic antibody (ACA), and circulating immune complexes (CIC) in schizophrenic patients.

Methods: A total of 30 drug-free schizophrenic patients and 42 healthy controls were enrolled in this study. T cell proliferation in response to PHA was measured using Methyl Thiazol Tetrazolium test. ANA and ACA were measured by indirect immunofluorescence. CIC concentration was determined using poly ethylene glycol precipitation assay.

Results: Mean PHA response was 1.96 +/- 0.83 in patients and 3.72 +/- 1.39 in healthy controls (p< 0.001). ANA and CIC concentrations were not significantly different between two groups. In addition, ACA was detected only in patients.

Conclusion: Increased production of ACA together with lower T cell response to mitogens in our patients provides evidence for the involvement of autoimmune mechanisms in the pathogenesis of schizophrenia.
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http://dx.doi.org/IJIv4i1A4DOI Listing
March 2007

Interferon-gamma gene polymorphism in Iranian patients with multiple sclerosis.

Iran J Allergy Asthma Immunol 2004 Sep;3(3):115-9

Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Interferon- gamma (IFN- gamma) is an important immune regulator and inflammatory cytokine which is implicated in the pathogenesis of multiple sclerosis (MS). A single nucleotide polymorphism, T to A, at position +874 in the first intron has previously been shown. This polymorphism is associated with IFN- gamma production level. To study the effect of this polymorphism on susceptibility to multiple sclerosis, we screened genomic DNA samples from clinically definite MS patients and their unaffected first-degree relatives as controls, using sequence-specific primers (PCR-SSP). The results indicated that MS patients showed a lower TT (21.2% vs. 30.3%) and higher AA (21.2% vs. 12.1%) genotypes compared to controls, although there were statistically no differences in the IFN- gamma genotype distribution between these two groups. Thus, our data indicate that there is no association between IFN- gamma +874 polymorphism and MS susceptibility or severity of the disease.
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http://dx.doi.org/03.03/ijaai.115119DOI Listing
September 2004