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Patients afflicted by diabetes mellitus (DM) usually have more infections than those without DM. The course of the infections is also more complicated in this group of patients. One of the possible causes of increased infections prevalence is a deficiency in the immunity. Besides some decreased cellular responses in vitro, no disturbances in adaptive immunity in diabetic patients have been described. Different disturbances (low complement factor 4, decreased cytokine response after stimulation) in humoral innate immunity have been described in diabetic patients. In this research hydrogen peroxide (reactive oxygen mediator) and nitric oxide (reactive nitrogen mediator) in the neutrophil and macrophage culture of peritone in rats were evaluated against C.albicans. Via intravenous injection of streptozocin (65 mg/kg), a diabetic rat model was obtained. nitric oxide and hydrogen peroxide assay was performed by the Griess and Walter-Ruch methods respectively. C.albicans colony count on SCC medium was also done in two groups of healthy and diabetic mice. Macrophages of the healthy group reacted to C.albicans severly compared to the diabetic group which significantly produced more nitric oxide (P0.028). Neutrophils of the healthy group produced more No compared to the diabetic group against C.albicans (P0.165). No considerable difference was observed in production of hydrogen peroxide by macrophages in two groups of healthy and diabetic mice. Neutrophils of the diabetic group produced more hydrogen peroxide compared to the healthy group (P1). There was no significant difference in C.albicans colony count between the two healthy and diabetic groups (P0.058). Although nitrogen and oxygen related factors are changed or reduced after diabetic induction, changes in other immune system factors cannot be undermined.

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Objective: HLA-G is a nonclassical major histocompatibility complex antigen and is expressed as seven isoforms, including four membrane bound (HLA-G1 to –G4) and three soluble (HLA-G5 to –G7) forms. The pattern of selective expression of HLA-G transcripts in tissues shows the existence of a tight transcriptional control on the gene expression. It has been revealed that cytokines including interfrons and IL-10 could cause stimulation of the HLA-G transcription. The purpose of this study was to examine the effects of IFN- on the expression of HLA-G transcripts in both PBMCs of normal and SLE patients. Materials and Methods: Whole blood of 20 female SLE patients and 15 healthy donor candidates for Bone Marrow Transplantation were used. PBMCs were isolated from the whole blood by Ficoll gradient centrifugation and cultured with or without IFN-/LPS for 48 hours. Total RNA was extracted from the cells by trizol method. After reverse transcription of RNA to cDNA and the performance of a multiplex PCR for beta actin and HLA-G, the PCR products were analyzed using electrophoresis on a 2 % agarose gel and stained with ethidium bromide. Results: The results showed that the transcription of HLA-G was higher in SLE patients compared to normal controls. Addition of IFN-/LPS could influence the expression of this molecule by increasing the transcription of HLA-G in both normal and patient PBMCs (P≤0.05). Conclusion: Transcription of HLA-G gene could be increased by the cytokine IFN-. This observation is in accordance with previous reports. This effect could be assigned to both normal and lupus Patients. The effects of the cytokine IFN-/LPS in the induction of HLA-G transcription were higher in normal than lupus patients. Nevertheless, the total expression of HLA-G was higher in lupus patients.

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Objective: Pseudomonas aeruginosa is the major cause of septicemia and wound infection in burned patients. Immunotraphy is the best practical way for prevention and treatment of these infections. Flagella as one of the most important bacterial virulence factors has important role in attachment, motility, chemotaxis and TLR-5-dependent immune response so that it propounded as a vaccine candidate. Production of anti-flagellar antibodies and evaluation of its protective effects in burned induced infection of mice was the main aim of this study. Materials and Methods: In the first step, flagellar antigen prepared by ultra-centrifugation. Anti-flagellar antibodies produced in rabbit and its impurity separated by absorption technique. Specification of the obtained antibodies for flagellar antigen was investigated via agglutination test. After determination of LD50 in a known strain, different dilutions of anti-flagellar antibodies injected in burned mice for passive immunization. The rate of bacterial spread from burn site was determined by quantification assay of bacteria in skin and liver. In this study, clinical isolate and PA103 in addition to ATCC 27853 strain were used for agglutination test. Results: H-antiserum reduced mortality of burned mice challenged with ATCC 27853 strains about 80%. Counting of bacteria in the skin and liver showed that the number of bacteria in immunized mice, in contrast with control group, was significantly low. Conclusion: The results of this study showed that anti-flagellar antibodies of Pseudomonas can inhibit invasion of Pseudomonas and facilitate its opsonization, so these antibodies have protective effects in burned wound infections.

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Objective: Cryptosporidiosis is a parasitic disease that is causing small protozoan genus Cryptosporidum and transmission take place through fecal- oral by direct contact or indirectly through food or drink. The aim of this study was detection of anti-Cryptosporidum parvum Immunoglobulin IgG, in newborn BALB/c infected with C. parvum. Materials and Methods: Oocysts of C. parvum were obtained from the feces of diarrheic lambs and following purification they were suspended in 2.5% aqueous potassium dichromate solution and stored at 4°C. Forty suckling BALB/c (3–4 days old) were divided in 8 groups (4 case groups and 4 control groups) each group consist of 5 suckling BALB/c. The mice in case groups were infected oraly with 105 C. parvum oocysts, and the mice in control groups served as non-infected. Blood samples were collected at 6, 9, 12 and 16 days post-infection (pi). Immunoglobulin IgG were extracted by salting out method and confirmed with SDS-PAGE. Results: Antibodies were analyzed by western blot and increased secretion of IgG was confirmed in neonatal mice infected with Cryptosporidum oocysts. Mean OD of Immunoglobulin IgG increased from 0.350 ± 0.099 to 0.6776 ± 0.099 in case groups but in control groups the increase was from 0.244 ± 0.016 to 0.322 ± 0.16 (P<0.05). Conclusion: The type of antibody in neonetal mice infected with Cryptosporidum oocysts was IgG which is secreted against external memberane of oocysts. Significant differences in neonatal mice case groups as compared with the control groups were observed.