Aryl hydrocarbon receptor gene expression in ankylosing spondylitis and its correlation with interleukin-17, RAR-related orphan receptor gamma t expression, and disease activity indices.

Objectives: Considering the role of T helper (Th)17 cells in the pathogenesis of ankylosing spondylitis (AS), the aim of this study was to determine the correlation between aryl hydrocarbon receptor (AHR) gene expression and the expression of Th17-related genes including interleukin (IL)-17 and RAR-related orphan receptor gamma t (RORγt) transcription factor. Patients and methods: Thirty patients with AS (26 males, 4 females; mean age: 36.1±8.1 years) and 30 age- and sex-matched healthy individuals (26 males, 4 females; mean age: 36.2±14.6 years) were recruited for the case-control study between June 2021 and January 2022. Ribonucleic acid (RNA) was extracted from peripheral blood cells and expression levels of AHR, IL-17, RORγt, and AHR repressor (AHRR) genes were evaluated using real-time polymerase chain reaction technique. The serum level of IL-17 was evaluated with enzyme-linked immunosorbent assay. Results: The results showed a nonsignificant elevation of AHR, IL-17, and RORγt gene expression in the patient group compared to the control. There was a direct correlation between AHR gene expression and IL-17 and RORγt genes and a negative correlation between AHR and AHRR expression. Moreover, AHR gene expression showed a weak correlation with disease activity indices, including Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Functional Index, Bath Ankylosing Spondylitis Metrology Index, Bath Ankylosing Spondylitis Global Score, and Ankylosing Spondylitis Quality of Life. Moreover, the serum level of IL-17 was higher in AS patients compared to the healthy group (p=0.02). Conclusion: Upregulated expression of the AHR gene in ankylosing spondylitis and its correlation with IL-17 and ROR-γ t gene expression suggests that it could be a potential diagnostic and therapeutic target for AS.

CBC Differences between Survived and Deceased COVID-19 Patients: A Cohort Study.

The Coronavirus disease 2019 (COVID-19) pandemic showed the importance of simple, low-cost, and accessible tests for patient triage. Complete Blood Count (CBC) can be considered a good option for predicting the prognosis of COVID-19 and daily follow-up of hospitalized patients. CBC tests of 100 COVID-19 patients admitted to the general ward or intensive care unit (ICU) were monitored for ten days. Routine laboratory tests were also performed. In addition, the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) were calculated at the time of admission. The WBC count of the ICU-admitted patients was significantly lower than in the non-ICU-admitted group (P = 0.008). The mean lymphocyte percentage of deceased patients was significantly lower than in the survived patients (P = 0.041), whereas the mean neutrophil percentage of the former group was higher than the latter ( P = 0.012). Moreover, the mean monocyte percentage of the survivors was significantly more than that of non-survivors (P = 0.003). However, there was no significant difference in mean platelet counts, hemoglobin levels, and red blood cell count between the studied groups. A lower WBC, lymphocyte percentage, and monocyte percentage, in addition to a higher neutrophil percentage, may indicate a poor prognosis in moderate to severe COVID-19 patients.

Circulating Exosomes and Ambient Air Pollution Exposure in COPD.

Background: Chronic obstructive pulmonary disease (COPD) is characterized by progressive obstruction of airways due to chronic inflammation. Both genetic and environmental components are risk factors for COPD. The most common cause of COPD is smoking. However, evidence suggests that 17% to 38% of COPD patients are nonsmokers, so other factors like air pollution may also play a role. Objective: The relationship between serum exosomes and exposure to particulate matter (PM) <2.5 and 10 micrometers (µm) in the residing environment of COPD patients and healthy groups was investigated. The correlation between inflammatory cytokine levels with exosome count was also studied. Methods: Peripheral blood samples were taken from 20 COPD patients without a smoking history or a family history of COPD, along with 20 nonsmoker healthy controls. The serum exosomes were counted by flow cytometry using a CD81 marker. The exposure to PM2.5 and PM10 was measured in daily, weekly, and monthly intervals based on the longitudinal measurements of the monitoring stations, and the correlation between exosome count and air pollutants was analyzed. Results: The serum CD81+ exosome count in COPD patients was significantly elevated compared to the healthy controls and this was correlated with daily PM10 (P-value=0.02) and monthly PM2.5 (P-value=0.02) exposure. Although interferon-gamma levels of COPD patients were higher than healthy controls, there was no correlation between exosome count and cytokine level. Conclusions: Considering the significant relationship between air pollutants and the count of serum exosomes demonstrated in the present study, air pollution might be a considerable risk factor in the progression of airway inflammation.

Percentage of Th1 and Th17 cells and serum level of IL-17 and IFN-γ cytokines in COVID-19-associated mucormycosis.

The considerable number of the 2019 coronavirus disease (COVID-19) patients who developed mucormycosis infections in West and Central Asia urged a need to investigate the underlying causes of this fatal complication. It was hypothesized that an immunocompromised state secondary to the excessive administration of anti-inflammatory drugs was responsible for the outburst of mucormycosis in COVID-19 patients. Therefore, we aimed to study the implication of two major subsets of adaptive immunity T helper (Th)-1 and Th17 cells in disease development. Thirty patients with COVID-19-associated mucormycosis, 38 with COVID-19 without any sign or symptom of mucormycosis, and 26 healthy individuals were included. The percentage of Th1 and Th17 cells in peripheral blood, as well as the serum levels of interleukin (IL)-17 and interferon-gamma (IFN-γ), were evaluated using flow cytometry and ELISA techniques, respectively. Th17 cell percentage in patients with COVID-19-associated mucormycosis was significantly lower than in COVID-19 patients (P-value: <0.001) and healthy subjects (P-value: 0.01). In addition, the serum level of IL-17 in COVID-19 patients was significantly higher than that of healthy individuals (P-value: 0.01). However, neither the frequency of Th1 cells nor the serum level of IFN-γ was different between the study groups. Given the critical role of Th17 cells in the defense against mucosal fungal infections, these findings suggest that low numbers of Th17 and insufficient levels of IL-17 might be a predisposing factor for the development of mucormycosis during or after COVID-19 infection.

Considering the critical role of Th17 cells in defense against mucosal fungal infections, the low numbers of Th17 and insufficient amounts of IL-17 might be a predisposing factor to develop mucormycosis during or after COVID-19 infection.

MicroRNAs-mediated regulation pathways in rheumatic diseases.

Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are two common rheumatic disorders marked by persistent inflammatory joint disease. Patients with RA have osteodestructive symptoms, but those with AS have osteoproliferative manifestations. Ligaments, joints, tendons, bones, and muscles are all affected by rheumatic disorders. In recent years, many epigenetic factors contributing to the pathogenesis of rheumatoid disorders have been studied. MicroRNAs (miRNAs) are small, non-coding RNA molecules implicated as potential therapeutic targets or biomarkers in rheumatic diseases. MiRNAs play a critical role in the modulation of bone homeostasis and joint remodeling by controlling fibroblast-like synoviocytes (FLSs), chondrocytes, and osteocytes. Several miRNAs have been shown to be dysregulated in rheumatic diseases, including miR-10a, 16, 17, 18a, 19, 20a, 21, 27a, 29a, 34a, 103a, 125b, 132, 137, 143, 145, 146a, 155, 192, 203, 221, 222, 301a, 346, and 548a.The major molecular pathways governed by miRNAs in these cells are Wnt, bone-morphogenic protein (BMP), nuclear factor (NF)-κB, receptor activator of NF-κB (RANK)-RANK ligand (RANKL), and macrophage colony-stimulating factor (M-CSF) receptor pathway. This review aimed to provide an overview of the most important signaling pathways controlled by miRNAs in rheumatic diseases.

Effect of Ramadan fasting on salivary IgA, serum IgA, IL-17, and IL-22 levels.

Background: nutritional factors might affect the number and function of immune cells for instance the production of cytokines and immunoglobulins. Ramadan fasting is intermittent abstinence from eating and drinking for almost four weeks. Aim: The present study aimed to investigate the influence of intermittent fasting on serum IgA, salivary IgA (sIgA), interleukin (IL)-17, and IL-22 levels. Methods: 40 healthy men aged 19-29 years were evaluated before and during the fourth week of Ramadan fasting for IgA levels by the nephelometric method as well as salivary IgA (sIgA), IL-17, and IL-22 amounts using enzyme-linked immunosorbent assay (ELISA). Results: serum IgA levels reduced significantly at the end of Ramadan fasting (225.8 ± 87 vs. 196 ± 70 mg/dl) (p-value<0.001); however, sIgA amounts did not differ between before and the last week of Ramadan. Serum IL-17 reduced significantly (2.93 ± 1.51 vs. 2.17 ± 1.33 pg/ml) (p-value = 0.006) whereas IL-22 levels remained approximately unchanged. Summary: four weeks of intermittent fasting during Ramadan reduced the serum levels of IgA and IL-17 but did not affect the production of sIgA and IL-22. These findings indicate a limited impact of intermittent fasting on mucosal immunity.

Expression of Programmed Cell Death 1 and Helios Genes Correlates With rs872071A>G and rs12203592C>T Single-Nucleotide Polymorphisms of InterferonRegulatory Factor 4 in Patients with T-Cell-Mediated Rejection of Renal Allograft.

OBJECTIVES: Acute T-cell-mediated rejection of the renal allograft is a serious posttransplant challenge that requires administration of high-dose immunosuppressive drugs with considerable side effects; therefore, specific targeting of T-cell responses may improve both prevention and treatment of T-cell-mediated rejection. A potential candidate for this purpose is interferon regulatory factor 4 because of its implication in differentiation and function of T cells. Our aim was to evaluate the frequency of the rs872071A>G and rs12203592C>T single-nucleotide polymorphisms of the interferon regulatory factor 4 gene and association of these 2 polymorphisms with the gene expression of programmed cell death 1 and Helios in patients with T-cell-mediated rejection versus stable recipients. MATERIALS AND METHODS: Sixty recipients with T-cell- mediated rejection and 60 age-matched and sex-matched stable recipients were recruited. Two single-nucleotide polymorphisms of interferon regulatory factor 4 gene, as well as the expression of programmed cell death 1 and Helios genes in peripheral blood mononuclear cells, were investigated with real-time polymerase chain reaction. RESULTS: Programmed cell death 1 gene expression was reduced in patients with T-cell-mediated rejection versus stable recipients (P = .03). The frequency of rs872071A>G and rs12203592C>T single-nucleotide polymorphisms showed no significant difference between groups. Presence of the rs12203592C>T single-nucleotide polymorphism was directly correlated with the expression of programmed cell death 1 gene (P = .049), and rs872071A>G positivity was directly correlated with Helios gene expression (P = .008), which suggests an inhibitory role for interferon regulatory factor 4 on programmed cell death 1 and Helios molecules. CONCLUSIONS: Programmed cell death 1 gene expression was lower in patients with T-cell-mediated rejection versus stable recipients. Low-expressing singlenucleotide polymorphisms of interferon regulatory factor 4 could enhance the downstream gene expression of programmed cell death 1 and Helios immunoregulatory molecules. Therefore, specific inhibition of interferon regulatory factor 4 may promote tolerance induction in the allograft.

Th17/Treg cell balance in stable liver transplant recipients.

BACKGROUND: Immune monitoring of transplanted patients may provide a reliable basis for the individualization of immunosuppressive therapy. In addition, it might be applied for realizing the early and non-invasive diagnosis of acute allograft rejection. METHODS: Percentages of TCD4 + IL-17+ (Th17) and TCD4 + CD25 + CD127dim/- (Treg) cells, as well as serum levels of interleukin (IL)-17 and transforming growth factor (TGF)-ß1, were evaluated in 30 stable patients using flow cytometry and ELISA techniques before and six months after liver transplantation. Besides, the same cells and cytokines were quantified in 10 recipients with acute allograft rejection. RESULTS: Six months post-transplant, the percentage of Th17 and Treg cells in the peripheral blood of stable liver transplant recipients reduced significantly, but the Th17/Treg ratios were comparable to the pre-transplant period (1.24 vs. 1.56); however, Th17/Treg ratios in the rejection group was significantly higher than in the stable recipients (4.06 vs. 1.56, P-value = 0.001). Stable patients showed decreased amounts of serum IL-17 which was remarkably lower than in the rejection group (P-value = 0.01). Moreover, there was a significant correlation between the serum level of IL-17 and the percentage of Th17 cells (P-value <0.001). Th17 frequency was negatively associated with the liver allograft function. Notably, TGF-ß1 levels differed neither between pre-and post-transplant samplings nor between stable and rejection groups. CONCLUSION: Six months after liver transplantation, the mean Th17/Treg ratio in stable recipients remained comparable to the pre-transplant values; however, it was significantly elevated in patients with acute allograft rejection, suggesting the Th17/Treg ratio as a probable predictor of acute rejection.

Potential cytotoxicity of PM2.5-bound PAHs and toxic metals collected from areas with different traffic densities on human lung epithelial cells (A549).

Laboratory and epidemiological researches have indicated that ambient air particulate matter have a plays critical role in causing diseases. The current research evaluated the chemical attributes of PM2.5 in the ambient air of the cities of Karaj and Fardis and determined its toxicological effects on human lung epithelial cells (A549). In the study city, 16 points were selected from the two high-traffic and low-traffic points for sampling. A sampling of ambient air was carried out in spring, summer, autumn, and winter 2018-19. Air sampling was performed for 24 h according to the EPA-TO/13A guidelines. To analyze of toxic metals and polycyclic aromatic hydrocarbons (PAHs), ICP-OES and GC-MS were used, respectively, and for cell toxicity analysis, an ELISA reader was used. Then from SPSS, Excel and R software were used for statistical analysis. The results of the current study indicated that the concentration of PAHs carcinogenic in the autumn season in high-traffic stations was the highest and equal to 9.3 ng/m3, and in the spring season in the low-traffic stations, it was the lowest and equal to 5.82 ng/m3. In general, during the period of study, Heavy metals including Zn, Fe, Pb, Cu, and Al had the highest concentration compared to other metals. However, Hg, Cr, As, Pb, Cu, Cd, and Zn were higher concentration in the winter and autumn seasons than in the spring and summer seasons. Cell viability measurements by using MTT showed that low-traffic and high-traffic stations had the highest toxicity in autumn season compared to other seasons. (p < 0.05). In general, high-traffic stations had the highest toxicity than low-traffic stations. The general conclusion of the present study was that PM2.5-bound PAHs and toxic metals, due to their high concentration, were toxic pollutants in air for residents of Karaj and Fardis. Also, the high concentration of PM2.5 caused the mitochondrial activity of A549 cells to stop and this stop was more significant in cold seasons and high-traffic areas.

Comparing IRF-4 Gene Expression Between Acute T cell- Mediated Rejection and Stable Renal Transplant Recipients.

INTRODUCTION: Renal transplant rejection is one of the clinical challenges, which usually requires administration of immunosuppressive drugs causing serious side effects. Therefore, invention of effective and specific therapeutics is necessary to control undesired immune responses particularly T-cell reactions to allograft. Interferon Regulatory Factor-4 (IRF-4) due to its implication on T cells differentiation and function might be targeted to treat T cell-mediated cellular rejection (TCMR). The aim of this study was to investigate the association between IRF-4 gene expression and acute TCMR, as well as to examine the correlation between IRF-4 gene expression and cellular expression of Programmed cell death-1 (PD-1) and Helios molecules. METHODS: Peripheral blood samples were obtained from 30 patients with biopsy proven acute TCMR and 30 stable recipients. IRF-4 gene expression was quantified using RT-PCR, and cellular expression of PD-1 and Helios were evaluated with flowcytometry. RESULTS: IRF-4 gene expression was significantly increased in acute TCMR patients compared with stable recipients (P < .05). Helios protein expression was slightly decreased in TCMR group but this was not statistically significant. There was a negative correlation between IRF-4 gene expression and PD-1 as well as Helios frequency in the whole studied population. CONCLUSION: IRF-4 expression increases in acute TCMR which might also lead to a diminished expression of downstream immunoregulatory molecules such as PD-1 and Helios. Therefore, specific inhibition of IRF-4 may be helpful in managing acute TCMR.

Adoptive Treg cell-based immunotherapy: Frontier therapeutic aspects in rheumatoid arthritis.

The major current focus on treating rheumatoid arthritis is to put an end to long-term treatments and instead, specifically block widespread immunosuppression by developing antigen-specific tolerance, while also permitting an intact immune response toward other antigens to occur. There have been promising preclinical findings regarding adoptive Treg cells immunotherapy with a critically responsible function in the prevention of autoimmunity, tissue repair and regeneration, which make them an attractive candidate to develop effective therapeutic approaches to achieve this interesting concept in many human immune-mediated diseases, such as rheumatoid arthritis. Ex vivo or invivo manipulation protocols are not only utilized to correct Treg cells defect, but also to benefit from their specific immunosuppressive properties by identifying specific antigens that are expressed in the inflamedjoint. The methods able to address these deficiencies can be considered as a target for immunity interventions to restore appropriate immune function.

Sirtuin 1: A Dilemma in Transplantation.

Sirtuin 1, a member of sirtuin family of histone deacetylase enzymes, has been implicated in a variety of physiologic and pathologic events, including energy metabolism, cell survival, and age-related alterations. In view of the anti-inflammatory properties of sirtuin 1 along with its protective role in ischemia reperfusion injury, it might be considered as contributing to the promotion of transplantation outcome. However, the potential ability of sirtuin 1 to induce malignancies raises some concerns about its overexpression in clinic. Moreover, despite the findings of sirtuin 1 implication in thymic tolerance induction and T regulatory (Treg) cells survival, there is also evidence for its involvement in Treg suppression and in T helper 17 cells differentiation. The identification of sirtuin 1 natural and synthetic activators leads to the proposal of sirtuin 1 as an eligible target for clinical interventions in transplantation. All positive and negative consequences of sirtuin 1 overactivation/overexpression in the allograft should therefore be studied thoroughly. Herein, we summarize previous findings concerning direct and indirect influences of sirtuin 1 manipulation on transplantation.

Proinflammatory effects of dust storm and thermal inversion particulate matter (PM10) on human peripheral blood mononuclear cells (PBMCs) in vitro: a comparative approach and analysis.

Particulate matter (PM) as the carcinogenic air pollutants can lead to aggravated health outcomes. Epidemiological studies demonstrated that PM can be engaged in different diseases such as cardiovascular, respiratory and cancer. The in vitro secretion of proinflammatory cytokines by human peripheral blood mononuclear cells (PBMCs) has been used to assess the effects of PM with an aerodynamic diameter < 10 µm (PM10). This study compared the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and interleukin 1-beta (IL1-ß) secretions of PBMCs exposed to PM10 of dust storm and inversion. We collected PM10 samples during the spring and autumn seasons in two locations. Isolated PBMCs were exposed separately to 50, 150, and 300 µg/ml of different type of PM10 for 4 and 24 h. The mean concentrations of TNF-α for the PM of dust storm and inversion were 6305.61 ± 2421 and 6651.74 ± 2820, respectively. Also the mean concentrations of IL1-ß for the PM of dust storm and inversion were 556.86 ± 162 and 656.35 ± 196, respectively. Furthermore, these values for the production of IL-6 were 12,655 ± 5661 and 16,685 ± 8069, respectively. Although no significant difference was observed between the PM of dust storm and that of inversion with regard to PBMCs, the results showed a significant increase in the proinflammatory cytokine secretion of both PMs compared with the controls. Moreover, TNF-α, IL1-ß, and IL-6 secreted in cells exposed to PM10 of dust storm were about 10 times more than the controls, these values for cells exposed to PM10 of inversion were around 10, 12, and 14 times more than the controls, respectively. It can be concluded that the PM10 of both dust storm and inversion can play a significant role in proinflammatory cytokine secretion due to its harmful effect on human health. Graphical abstractThis picture shows the Proinflammatory cytokine producing potential of PM10 with two sources (dust storm and urban air pollution) in exposure with human PBMCs in vitro.

Correction to: Chemical composition of PM10 and its effect on in vitro hemolysis.

[This corrects the article DOI: 10.1007/s40201-018-00327-w.].

Chemical composition of PM10 and its effect on in vitro hemolysis of human red blood cells (RBCs): a comparison study during dust storm and inversion.

PURPOSE: This study aimed to investigate chemical composition of PM10 (particulate matter with aerodynamic diameter ≤ 10 µm) during dust storm and inversion in Tehran and hemolysis effects. METHODS: PM10 was sampled in Tehran, Iran, during dust storm and inversion conditions. Water soluble ions (F¯, Cl¯, NO2¯, NO3¯, SO4¯2, Na+, K+, NH4 +, Ca+2, Mg+2) and elements (Al, Ba, Cd, Co, Cr, Cu, Fe, Li, Mn, Mo, Ni, Pb, Se, Sn, Sr, V, Zn, Pt, Rh, Pd, As and Si) were analyzed by ion chromatograph (IC) and inductively coupled plasma optical emission spectrometer (ICP-OES), respectively. Hemolysis was examined as in vitro at PM10 concentrations of 50-300 µg/ml. RESULTS: Daily average of PM10 concentrations in dusty and inversion days were 348.40 and 220.54 µg/m3, respectively. Most prevalence ionic components were NO3¯, Cl¯, SO4¯2 and Ca+2 during dust storm and SO4¯2, NO3¯, Cl¯ and NH4 + during inversion. Si, Fe and Al had the maximum values in both conditions. Particles associated with both conditions induced hemolytic responses. PM10 from dusty day showed a higher hemolysis percent (10.24 ± 4.67%) than inversion (9.08 ± 5.47%), but this difference was not significant (p = 0.32). Hemolytic effects were significantly intensified by increased PM concentrations (p < 0.001) in a dose-response manner. CONCLUSIONS: As the results, chemical composition of sampled particles from inversion days and dust storm was different from each other. Hemolytic effects of particles during dust storm were more than inversion days. However, this difference was not statistically significant.

Effect of food intake and ambient air pollution exposure on ankylosing spondylitis disease activity.

BACKGROUND: Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by axial arthritis. The genetic-environmental factors seem to be involved in the pathogenesis of the disease and the disease debilitates patients during the most productive stages of their lives. The aim of this study was to examine the relationships between two environmental factors, diet and air pollution with disease activity and functional impairment in AS. METHODS: A case-control study was carried out. Thirty patients with AS and 30 age and sex-matched healthy controls were included. Disease scores including BASMI, BASDAI, BASFI, and BASG were calculated by means of the international Ankylosing Spondylitis Assessment working group consensus recommendations. The food intake was evaluated by semi-quantitative food frequency questionnaire (147 items FFQ). Level of air pollution indices, PM10 and PM2.5 information was obtained from the Tehran air quality control network. RESULTS: Total energy and fat intake, some vitamins (A, B1, B2, C) and mineral intake (potassium, calcium, iron, phosphorus, magnesium, zinc, copper and selenium) were significantly higher in patients with AS compared to controls. Fat component consumption especially Saturated Fat of Food was moderately correlated with BASFI score. PM2.5 long term exposure was strongly correlated with BASMI, BASFI and BASDAI scores of patients. CONCLUSION: High-fat diet and long term exposure to air pollution are associated with worse disease outcomes reported in patients with AS. This is an interesting area of investigation in AS pathogenesis and management.

Gene therapy in rheumatoid arthritis: Strategies to select therapeutic genes.

Significant advances have been achieved in recent years to ameliorate rheumatoid arthritis (RA) in animal models using gene therapy approaches rather than biological treatments. Although biological agents serve as antirheumatic drugs with suppressing proinflammatory cytokine activities, they are usually accompanied by systemic immune suppression resulting from continuous or high systemic dose injections of biological agents. Therefore, gene transfer approaches have opened an interesting perspective to deliver one or multiple genes in a target-specific or inducible manner for the sustained intra-articular expression of therapeutic products. Accordingly, many studies have focused on gene transferring methods in animal models by using one of the available approaches. In this study, the important strategies used to select effective genes for RA gene therapy have been outlined. Given the work done in this field, the future looks bright for gene therapy as a new method in the clinical treatment of autoimmune diseases such as RA, and by ongoing efforts in this field, we hope to achieve feasible, safe, and effective treatment methods.

Single Nucleotide Polymorphisms of PTPN22 Gene in Iranian Patients with Ulcerative Colitis.

OBJECTIVES: Protein tyrosine phosphatase non-receptor type 22 gene (PTPN22) single-nucleotide polymorphisms (SNP) have been associated with a number of different autoimmune diseases. This study aimed to investigate the association of five polymorphisms of PTPN22 gene with susceptibility to ulcerative colitis (UC) in Iran. MATERIALS AND METHODS: A total of 67 patients diagnosed with UC (35 female and 32 male all under 18 years) and 93 healthy subjects were selected. The samples were genotyped for the, rs12760457, rs2476601, rs1310182, rs1217414, and rs33996649 in PTPN22 gene using real-time polymerase chain reaction (PCR) allelic discrimination TaqMan genotyping assays. RESULTS: The frequencies of the rs1310182 A and G alleles, and also the AA and GG genotypes were significantly different between the patient and the control groups (p < 0.05). The carriage of G allele of rs1310182 was significantly associated with increased risk of UC (OR (95% CI) = 1.17 (0.70-1.98), p < 0.001). Moreover, the genotype GG of SNP rs1310182 was significantly associated with UC (OR (95% CI) = 2.32 (1.13-4.76), p < 0.01). No association was found between other PTPN22 gene SNPs among UC patients. CONCLUSION: PTPN22 gene polymorphism in rs1310182 could play a crucial role in susceptibility to UC.

Investigation and Comparison of In Vitro Genotoxic Potency of PM10 Collected in Rural and Urban Sites at Tehran in Different Metrological Conditions and Different Seasons.

The particulate matter has become a serious health problem in some large cities in the world. These particles are a complex mixture of chemical compounds which change based on location and time and, consequently, can cause different health-related effects. The exact mechanism of the effect of these particles is not yet known for certain. However, it seems that numerous mechanisms through the production of ROS and, eventually, DNA destruction, which are related to a wide range of diseases, are among the causes of particles' health-related effects. The present study is aimed to evaluate and compare the genotoxicity potential of particles collected in Tehran, Iran, in urban and rural regions during spring and autumn as well as dusty and inversion conditions. These effects were examined using the comet assay on human pulmonary epithelial cells (A549). Results showed that all the particles had the potential for genotoxicity at the concentration used in this study (75,150 and 300 µg/ml). Moreover, DNA destruction changed with season, site, and even dusty and inversion atmospheric conditions. These changes mostly belonged to urban particles. In general, urban particles in autumn and, specifically, on days with inversion had higher genotoxicity (p < 0.01). Difference was observed between dusty and regular days so that regular days were more potent (p < 0.05). A strong correlation was observed between the effects of most PAH compounds and other metals such as Cr, Co, Cd, Mn, As, and also SO4, which were mostly the result of combustion in vehicle engines in urban regions. No difference was observed for rural particles at different conditions and seasons.

Correction to: Investigation and Comparison of In Vitro Genotoxic Potency of PM10 Collected in Rural and Urban Sites at Tehran in Different Metrological Conditions and Different Seasons.

The original version of this article unfortunately contained a mistake. Figure 6 caption should be "The light microscopic image (a) and transmission electron microscopic image (b) of A549 cell after 24 h of exposure to PM10 (150 µg/ml).