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Showing 7 results for Cytokines
The effects of different periods of renal ischemia/reperfusion injury on rats’ liver function, cytokine levels and antioxidant status
Kadkhodaee M, Golab F, Zahmatkesh M, Ghaznavi R, Hedayati M, Arab Ha, Soleimani M,
Volume 67, Issue 7 (10-2009)
Abstract

Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: The effect of ischemia/reperfusion (I/R) injury on kidney has been under investigation for many years. But the changes in liver function and oxidative stress status in renal I/R injury is not well known. Recent studies suggest a crosstalk between liver and kidneys. The aim of the present study was to assess liver changes after induction of various degrees of renal I/R injury.
Methods: This is an experimental study conducted on 20 male rats that were obtained from animal house of Physiology Department. Twenty male rats were subjected to either sham operation or ischemia (30, 45 and 60 min) followed by 60 min reperfusion periods. Blood samples were drawn post-operatively and plasma creatinine, BUN, ALT and AST were measured. Hepatic glutathione (GSH) and FRAP (ferric reducing antioxidant power) levels and the concentration of IL-10 and tumor necrosis factor (TNF) -alpha were evaluated.
Results: Both 45 and 60 min ischemia followed by 1h reperfusion periods resulted in significant increases in plasma creatinine (11.1±1.7mg/dl and 1.24±0.07mg/dl vs 0.55±0.15mg/dl, p<0.05) and BUN (34±3.85mg/dl and 35.0±2.81mg/dl vs 23.75±1.1mg/dl, p<0.05). These rats showed a significant decrease in liver GSH as well as significant increase in TNF-a & IL-10 concentrations.
Conclusion: Renal ischemia causes changes in liver function and oxidative stress status. A minimum of 45 min ischemia is needed to study the effects of renal injury on liver as a remote affected organ.


The comparison of TH1 and TH2 cytokines gene expression in allergic and non-allergic patients with nasal polyps by PCR
Farhadi M, Tabatabaee A, Shekarabi M, Noorbaksh S, Khatib M, Javadinia Sh,
Volume 69, Issue 9 (12-2011)
Abstract

Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: Too many studies are in the process of determining the probable role of immune system in the etiopathogenesis of nasal polyposis. This study was designed to identify the probable participation of Th1, Th2 lymphocytes in the induction and progression of nasal polyposis.
Methods:  Seventy-five patients, 42 male and 33 female, with nasal polyposis were examined for total serum IgE, specific serum IgE and reaction to skin test for differentiating allergic from non-allergic participants in Rasoul Akram Hospital during 2010. To determine the possible correlation of allergic reactions in the upper respiratory tract and nasal polyposis, cytokine gene expression was evaluated on the extracted RNA by RT-PCR. The data were analyzed by using c2, independent t-test, correlation and Receiver operating characteristic (ROC) curve.
Results:  The mean age of participants was 38 years (18-81 years). IFN-γ and IL-4 gene expressions were more prevalent in allergic than non-allergic individuals (IFN-γ: 39.5% vs. 14.2%, P=0.3 and IL-4: 44.7% vs. 18.9%, P=0.02, respectively). IL-10 and IL-12 (P35 and P40 fractions) genes were not significantly different between the two groups. IL-10 and IL-12 (P35, P40) genes did not differ significantly either.
Conclusion: This research suggests that overproduction of cytokines and an imbalance of Th1 and Th2 cell production may play an important role in the pathophysiology of allergic or non-allergic nasal polyp formation. Thus, although nasal polyposis is a multifactorial disease with several different etiological factors, chronic persistent inflammation is undoubtedly a major factor irrespective of the etiology.


Role of the immune cells, mediators and cytokines in pathogenesis of asthma: a review article
Sedigheh Bahrami Mahne, Seyed Alireza Mahdaviani , Nima Rezaei ,
Volume 72, Issue 5 (8-2014)
Abstract
Asthma is a chronic inflammatory disorder of the airways, associated with airway re-modeling and hyperresponsiveness. It is expressed that asthma influences about 300 million people around the world, which is estimated to increase to about 400 million by 2025. The prevalence rate is 15 to 20 percent in children and 5 to 10 percent in adults, while its trend is still increasing. Inflammation plays an important role in the patho-physiology of asthma, which involves an interaction of different types of the immune cells and mediators. It leads to a number of pathophysiology changes, including bron-chial inflammation, airway obstruction, and clinical episodes such as cough, wheeze and shortness of breath. Asthma is now greatly being introduced as a heterogeneous disorder and it is pointed out to the role of T cells, including Th1, Th2, Th17, and regu-latory T cells. Other immune cells, especially neutrophils, macrophages and dendritic cells, as well structural cells such as epithelial and airway smooth muscle cells also pro-duce disease-associated cytokines in asthma. Increased levels of these immune cells and cytokines have been recognized in clinical samples and mouse models of asthma. Different cytokines, including pro-inflammatory cytokines (such as TNFα, IL-1, and IL-6), T helper 2 cytokines (such as IL-4, IL-5, IL-9, IL-13), and growth factors (such as GM-CSF, PDGF) play a role in the pathogenesis of asthma. Indeed chemokines (such as MPC-1, RANTES , MIP-1) and the chemokine receptors (such as CCR3, CCR4, CCL11, CCL24, and CCL26) play an important role in the recruitment of circu-lating inflammatory cells into the airways in asthmatic patients and also is related with increased T helper 2 cytokines after inhaled allergens. Among new approaches, treat-ment of asthma with anti-cytokine drugs such as antibodies blocking IL-4, IL-5, IL-9 could reduce recruitment inflammatory cells into the airways and remodeling. The final perspective of asthma treatments would be to alter from the symptomatic treatments to disease modifying.
Effect of mesenchymal stem cells on allergic asthma in mouse model
Reza Habibian , Nowruz Delirezh , Amir Abbas Farshid ,
Volume 73, Issue 5 (8-2015)
Abstract
Background: Allergic Asthma is an inflammatory disease of the respiratory system that is well known by increased inflammatory cells in the airways and causes difficulty in respiration. The prevalence of allergic asthma is increasing worldwide, and it has become a significant cause of health challenge especially in developed countries. Inhaled β2-agonists and Inhaled or oral corticosteroids are common medications for treating the disease, but they cannot be used for long periods of time because of frequently occurring side effects and they can’t change the main pathogenesis of the problem. Deficiency in regulatory system against inflammation could be an important factor in allergic asthma. Mesenchymal stem cells (MSCs) have potential of cellular immunosuppressive therapy of inflammatory disorders. The aim of present study was to evaluate the effects of MSC therapy on mechanisms of allergic asthma in mice model. Methods: This experimental study was conducted from August 2014 to March 2015. The animals were housed and maintained in Biotechnology Center of Urmia University, Iran. Mice were sensitized by intra-peritoneal injection of ovalbumin (OVA) and aluminum hydroxide emulsion and then were challenged intra-nasally with OVA. Before allergen challenge on day 14, experimental mice received tail vein injection of MSCs in PBS. Regulatory T cells of spleen, cytokines and IgE analysis were carried out using lungs wash as well as serum samples. Results: Our results showed that MSCs significantly reduced total cells and eosinophilia, serum OVA-specific IgE concentration in OVA-sensitized and challenged mice. Also results showed that MSCs markedly inhibited expressions of Th2 cytokines and elevated levels of Treg cells and Treg cytokines. Conclusion: In the present study, we demonstrated the inhibitory effect of MSCs on airway inflammation using mice model of allergic asthma. The mice were sensitized with OVA and compared to the results of dexamethasone administration. Our results demonstrated that administration of MSCs could be used as a potential therapeutic approach for the allergic asthma.
The role of cytokines in systemic lupus erythematosis: review article
Shideh Namazi , Vahid Ziaee , Nima Rezaei ,
Volume 73, Issue 6 (9-2015)
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, involves almost all organs such as skin, heart, kidneys and central nervous system. The disease is characterized by vascular and connective tissue inflammation in a recurring pattern of remission and flare. Although the exact pathophysiology of disease has not been fully understood yet, the fundamental defect in SLE is attributed to dysfunction of T lymphocytes in controlling of B-cell that leads to polyclonal activation of B lymphocytes and production a large quantity of autoantibodies against nuclear and cytoplasmic components. These autoantibodies can damage tissues either directly or as a result of immune complex deposits. Several factors are involved in pathogenesis of SLE which can be divided into three major groups, environmental factors, genetic components, and immunological disturbances. They could breakdown body tolerance towards endogenous antigens and cause abnormal immunologic response to the healthy tissue, resulting in tissue damage. SLE occurs more frequently in female than male. It seems that immunological factors have important role in SLE. Inflammation and vascular endothelium irregularities are a number of main pathologies seen in SLE. Cytokines are protein mediators that play an essential role as regulator of innate and adaptive immune response against microbial agents or self-antigens. Influences of cytokines in autoimmune diseases such as SLE are poorly understood. Studies in both experimental animal models of lupus and patients with SLE have revealed a number of cytokine pathways that are important in the disease process. These studies showed that overexpression of inflammatory cytokines increases the proliferation of auto reactive B-cells and results in higher production of autoantibodies. Among them, the role of B-cell activating factor (BAFF), a proliferation-inducing ligand (APRIL), TNF-α, IFN-α, IL-6, IFN-γ, IL-23/IL-17, IL-10, IL-21 are prominent, which is associated with the generation of pathogenic autoantibodies and formation of immune complexes. In this paper, the role of cytokines and their encoding genes are described, while therapeutic applications are also briefly presented.
Gene cloning and expression of soluble thrombopoietin functional domain by harnessing Rosetta-gami expression system
Mohammad Moradi , Kamran Atarodi , Mahshid Mohammadipour , Kamran Mousavi Hosseini ,
Volume 76, Issue 6 (9-2018)
Abstract
Background: Thrombopoietin (TPO) is an important cytokine that has a critical role in regulating hematopoietic stem cells (HSCs) proliferation and megakaryocyte differentiation. Because of scares amount of this protein in human plasma, in many biotechnological centers around the world, recombinant production of this protein has been carried out. This study was aiming to gene cloning and expression of recombinant thrombopoietin.
Methods: This research is an experimental laboratory study carried out in Blood Transfusion Research Center, Tehran, Iran, from July 2016 to August 2017. At the beginning HepG2 cell line was cultured and RNA extraction was performed. Extracted RNA was used as template for cDNA synthesis and subsequently the synthesized cDNA was adopted to isolate TPO gene through polymerase chain reaction (PCR) reaction using designed primers. After isolating the TPO sequence from HepG2 cell line, the designated sequence was inserted into pET32 vectors. Recombinant plasmid was amplified by meriting from DH5α replicating system. The amplified plasmids were sequenced via chain termination method. Next step was transforming the recombinant plasmid into Rosetta-gami bacteria to express the recombinant protein. In order to induce protein expression, an appropriate amount of isopropyl β-D-1-thiogalactopyranoside (IPTG) was added to growth media, then bacterial lysate of expression host was prepared and assayed via polyacrylamide gel electrophoresis and western blotting test.
Results: After sequencing of recombinant plasmid, it was confirmed that TPO sequence has been successfully colonized in adopted vector. Subsequent to induction of recombinant protein, total cell protein analysis affirmed that recombinant protein has been expressed in its soluble form at cytoplasmic condition. Location of expected recombinant protein band on polyacrylamide gel and reaction of recombinant protein with His-tag monoclonal antibody at western blotting was asserting that expressed protein is the one of interest.
Conclusion: Rosetta-gami bacteria has capability of expressing recombinant thrombopoietin in its soluble form. By harnessing this method of recombinant protein expression, it would be possible to take advantage of high throughout bacterial expression system which would not produce inclusion body and its product doesn’t need further processing and refolding.

The effect of enalapril on pro-inflammatory cytokines in patients with migraine: a double-blind, randomized clinical trial
Shaghayegh Haghjooy Javanmard, Seyed Ali Sonbolestan , Kiyan Heshmat ,
Volume 77, Issue 3 (6-2019)
Abstract
Background: One of the possible mechanisms of migraine pathophysiology is neuro inflammation in which, according to previous studies, some changes happen in inflammatory factors like interleukins, adhesion molecules or acute phase reactants. Cytokines may have an essential role in the neurovascular inflammation and also in the process of pain especially in migraine patients. On the other hand, one of the mechanisms by which angiotensin converting enzyme inhibitors (ACEIs) work is anti-inflammation. The goal of this study was to evaluate the effect of enalapril as an ACEI drug, on the proinflammatory cytokines (calcitonin gene-related peptide (CGRP), tumor necrosis factor alpha (TNFα)) of migraine patients.
Methods: In this randomized double blind placebo-controlled clinical trial, 40 migraine without aura patients (mean age of 34.42±1.82 years) who were referred to neurology clinics of Isfahan University of Medical Sciences, Iran, between June 2011 and July 2012 were recruited. The patients were randomly divided into two groups. 21 patients were treated with 10 mg enalapril daily for two months as the intervention group and they were compared with matched placebo treated group of 19 patients. Serum samples were collected from all of the subjects and TNFα and CGRP levels were measured by means of ELISA (enzyme-linked immunosorbent assay) kits at the beginning of study (before the intervention) and after 2 months of enalapril or placebo treatment. The serum levels were compared in each group and between the groups. SPSS software, version 16 (SPSS Inc., Chicago, IL, USA) was used for statistical analysis.
Results: Six males (15%) and 34 females (85%) were enrolled in this study. The mean of migraine history among the subjects was 74.40±7.54 months. Patients' TNFα level decreased significantly in the case group after treatment with enalapril (P=0.001) while there was no significant change in control group (P=0.769). There was no significant difference in the CGRP concentrations in the intervention and control groups (P=0.795, 0.708 respectively).
Conclusion: Enalapril may be effective in improvement of inflammatory responses of migraine patients by decreasing the inflammatory factors like TNFα.

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