The effects of extremely low-frequency electromagnetic fields on c-Maf, STAT6, and RORα expressions in spleen and thymus of rat.

The study investigated the effect of extremely low-frequency electromagnetic fields (ELF-EMFs) exposure at different magnetic flux densities on genes expression of transcription factor Maf (c-Maf), signal transducer and activator of transcription 6 (STAT6), and retinoid-related orphan receptor alpha (RORα) in the spleen and thymus of rats. Eighty adult male rats were separated into four ELF-EMFs exposed and were exposed to magnetic flux densities of 1, 100, 500, and 2000 µT at a frequency of 50 Hz for 2 h daily for up to 60 d. All rats were intraperitoneally immunized on d 31, 44, and 58 of exposure. The experimental results showed that the expression levels of c-Maf, STAT6, and RORα in the thymus were not significantly changed at different magnetic flux densities. The expression levels of RORα and c-Maf were significantly downregulated at the densities of 1 and 100 µT, while the expression of STAT6 was only significantly decreased at the density of 100 µT. In conclusion, low magnetic flux densities of ELF-EMFs may reduce the expression levels of c-Maf, STAT6, and RORα genes in the spleen.

Detection of Toxoplasma gondii B1 gene in placenta does not prove congenital toxoplasmosis.

BACKGROUND: Congenital toxoplasmosis is an important disease that occurs when pregnant women become infected with Toxoplasma gondii during pregnancy. The aim of this study was to investigate the presence of T. gondii B1 gene in placental tissues of IgM seronegative women. MATERIALS AND METHODS: In this research, chronic toxoplasmosis was identified through examination of blood samples in a group of pregnant women by anti-Toxoplasma IgG and IgM ELISA and nested-PCR techniques. IgG avidity test was used to estimate the onset of infection in some pregnant women with chronic infection. After delivery, some umbilical cord and neonatal blood were tested by anti-Toxoplasma IgM ELISA, and also the B1 gene of T. gondii was investigated in their placental tissue by nested-PCR. Some factors such as blood sampling time and some clinical symptoms experienced during pregnancy were recorded. RESULTS: One hundred and sixty seven out of 653 (25.6%) pregnant women were positive for anti-Toxoplasma IgG. Of them, 165 (98.8%) were negative for anti-T. gondii IgM. Six out of 10 (60%) placental tissues from IgG seropositive, IgM seronegative women were positive for T. gondii B1 gene, while anti-Toxoplasma IgM was negative in the umbilical cord and neonatal blood samples. The results of IgG avidity test showed low avidity in one and high avidity in two women's samples. The B1 gene was not found in the blood samples of any of the six mothers. The most symptoms experienced during pregnancy were headache and nausea. CONCLUSION: The detection of B1 gene in placental tissues of the healthy newborn infants reiterates that presence of T. gondii in the placenta does not always result in congenital toxoplasmosis.

Evaluation of Toxoplasma gondii B1 gene in Placental Tissues of Pregnant Women with Acute Toxoplasmosis.

BACKGROUND: One of the consequences of toxoplasmosis is the risk of passing it from mother to fetus and the onset of congenital toxoplasmosis during pregnancy. The purpose of this study was to evaluate the B1 gene of Toxoplasma gondii in the placental tissues of pregnant women with acute toxoplasmosis. MATERIALS AND METHODS: The study was a cross-sectional study. Serum samples of pregnant women who attended to Fatemieh Hospital of Hamadan University of Medical Sciences were tested for immunoglobulin G (IgG) antibodies against T. gondii by enzyme-linked immunosorbent assay. Then, polymerase chain reaction was used to identify the specific B1 gene of T. gondii in IgG seropositive women. The placental tissues of the pregnant women with positive serum B1 gene examined for this gene. Anti-Toxoplasma immunoglobulin M (IgM) was performed on the umbilical cord and neonate blood. RESULTS: Anti-Toxoplasma IgG was detected in 167 out of 653 (25.6%) pregnant women. T. gondii B1 gene was identified in 36 out of 167 (21.6%) of IgG seropositive women. After delivery, the B1 gene was evaluated in 15 out of 36 (41.7%) patients' placental tissues, 13 of which were positive for this gene (86.7%). Anti-Toxoplasma IgM was detected neither in any umbilical cord nor in neonatal blood samples. All newborns, with the exception of one case, were born with normal birth weight and in term birth. CONCLUSION: The B1 gene was detected in 86.7% of the placental tissue of women who were involved in acute toxoplasmosis during pregnancy.

Evaluation of interleukin 8 +2767 A/T polymorphism in visceral leishmaniasis.

OBJECTIVE: To evaluated the relationship between the genetic variations at IL-8 +2767 position with VL pathogenesis among Iranian patients. METHODS: Three groups including patients with VL clinical presentation and leishmania seropositive (n = 124), patients seropositive but without clinical presentation (n = 82) and healthy controls (n = 63) were selected to conduct this cross-sectional study. Polymorphism at +2767 position of IL-8 was investigated using PCR-RFLP techniques. Anti-leishmania antibody titration was evaluated by the immunoflorescence technique. RESULTS: We observed higher significant frequencies +2767 A/A and A/T genotypes in Group 1 compared to Group 2 and healthy controls (P = 0.001). Also, patients in Group 1 carrying A/A genotype showed higher titer of anti-leishmania antibody than patients with A/T and T/T genotypes (P = 0.05). The validity of the data was analyzed using Hardy-Weinberg equilibrium and one way analysis of variance (ANOVA), as well as χ2 tests. CONCLUSIONS: Our findings indicate that the IL-8 +2767 polymorphism is significantly involved in impaired immune responses against VL and it could be considered as a risk factor for the VL progress.

Interleukin-4 receptor alpha T1432C and A1652G polymorphisms are associated with risk of visceral leishmaniasis.

BACKGROUND: Immune responses play significant roles in protection against leishmaniasis. Polymorphisms within the interleukin 4 receptor alpha chain (IL-4Rα) gene affect the production of cytokines, which is important for the clearance of many pathogens. The aim of the current study was to identify the relationship between visceral leishmaniasis (VL) infection and polymorphisms at positions T1432C and A1652G of IL-4Rα in an Iranian population. MATERIALS AND METHODS: This cross-sectional study was performed during 2004-2012 and included three groups of participants: VL patients (Group 1, n = 124), seropositive healthy controls (Group 2, n = 101), and seronegative healthy controls (Group 3, n = 55). The IL-4Rα T1432C and A1652G polymorphisms were evaluated using a polymerase chain reaction-restriction fragment length polymorphism technique, and anti-Leishmania antibody titers were determined by using immunofluorescence technique. Alleles and genotypes were compared between groups of the study as well as Groups 1 and 2 based on the titer of antibodies. The validity of the data was analyzed using Hardy-Weinberg equilibrium and one-way analysis of variance, as well as χ (2) tests. RESULTS: The polymorphisms at IL-4Rα positions T1432C and A1652G were significantly associated with active VL infection. These results demonstrated that the IL-4Rα T1432C and A1652G polymorphisms were not associated with anti-Leishmania antibody production. CONCLUSION: Our results indicate that these IL-4Rα polymorphisms may be risk factors for the development of VL.

Evaluation of interleukin-8 -251 t/a polymorphisms in visceral leishmaniasis.

BACKGROUND: Interleukin (IL)-8 plays important roles in the recruitment and activation of immune cells during visceral leishmaniasis (VL). Genetic variations in IL-8 modulate the expression of IL-8 protein and may be associated with VL. This study aimed to evaluate polymorphisms at the IL-8 -251 position in VL patients. METHODS: This cross-sectional study was performed on three groups: Leishmania-seropositive patients with clinical symptoms of VL (n = 91), seropositive patients without clinical symptoms (n = 104), and healthy controls (n = 110). Polymorphisms at the IL-8-251 position were analyzed using allele-specific polymerase chain reaction (PCR). Anti-Leishmania antibody titers were assessed by immunofluorescence. RESULTS: IL-8-251 polymorphism was significantly associated with VL (P<0.002). The IL-8-251 T/T genotype was significantly higher in group 1 than in groups 2 and 3 (P<0.002). The validity of the data was analyzed using Hardy-Weinberg equilibrium and one-way analysis of variance (ANOVA), as well as χ2 tests. CONCLUSIONS: IL-8-251 polymorphism was significantly associated with impaired immune responses in VL and might be considered a risk factor for disease development.

The L-selectin Phe206Leu gene polymorphism is not associated with visceral leishmaniasis.

BACKGROUND: Previous studies revealed that selectins play key roles in homing of immune cells to inflamed tissues and lymphatic organs. L-selectins are expressed on immune cells and interact with P and E selectins to homing to the tissues, hence, the polymorphisms within the gene of L-selectins may are associated with alteration in its expression. Thus, the current cross-sectional analytical study has been designed to investigate the polymorphisms within L-selectin gene and their relation with visceral leishmaniasis (VL). METHODS: This study was performed on 194 samples during 2004-2012.The PCR-SSP and immunoflorescence techniques were used to evaluate the L-selectins polymorphism and anti-Leishmania antibody titration, respectively, in 56, 74 and 64 seropositive VL patients (group 1), seropositive healthy controls (group 2) and seronegative healthy controls (group 3). RESULTS: The results showed that the genotypes (P=0.711) and alleles (P=0.679) within L-selectins gene (A/C) was not differ between groups. Our results also demonstrated that the genotypes within L-selectins in group 1 (P=0.807) and 2 (P=0.441) were not associated with the titration of anti-leishmania antibody. CONCLUSIONS: The results identified that the polymorphisms within L-selectins gene were not associated with VL and it may be concluded that these genotypes and alleles are unable to affect immune responses in VL patients.