[Chitosan nanopolymers effect in activating of mouse bone marrow derived dendritic cells]

Background and Aim: Regarding to various problems in the activation of dendritic cells and immune system's responses, finding of a safe, effective and applicable agent is highly desirable. Chitosan is an effective gene delivery agent and also a part of nanoscaffolds. In the present study, chitosan nanopolymers effect on dendritic immune cells were assessed

Materials and Methods: In this experimental-laboratory study, chitosan [150 KD] in acetic acid 1% solution was depolymerized to 10 KD oligomers using NaNO2. The oligomers particles were obtained by means of 2 normal NAOH molecules. Denderitic cells were derived from the rats' bone marrow using GM-SCF. On the treated denderitic cells CD40, CD86 and MHC-II maturation markers were evaluated by flowcytometery and TNF-alpha release was evaluated using ELISA method and T cell proliferation

Results: It was observed that dendrtic cells purity on the 8th day was more than 90%. Flowcytometery analysis showed an increase in all evaluated CD40, CD86 and MHC-II maturation markers [p<0.05]. TNF-alpha release and T cell proliferation significantly increased by chitosan treated denderitic cells compared to unstimulated or lipofectamin treated cells [P<0.05]

Conclusion: Results showed that chitosan nanopolymers significantly increased dendertic cell maturation phenotype, proinflamatory cytokine production, and induction of T cell proliferation. Therefore, chitosan nanocomplexes and scaffolds can induce and accelerate immune responses

Polymorphisms within exon 9, but not intron 8, of the vitamin d receptor gene are associated with Asthma

Deregulation of the immune system through allied factors and cytokine responses are thought to be important contributors to the pathogenesis of asthma. Vitamin D3 and its nuclear receptor appear to be factors that maybe involved in regulating i mmune responses during the progression of asthma. The aim of this study was to investigate the association between polymorphisms in intron 8 and exon 9 of the vitamin D receptor [VDR] and this disease. This study was performed on 100 asthmatic patients and 100 healthy controls. PCR-RFLP was performed to examine polymorphisms in intron 8 and exon 9 of VDR gene. Our results showed a statistically significant difference in the Taq-1 evaluated genotypes of exon 9 of the VDR gene when comparing healthy patients to asthmatic patients. Based on our results, it can be concluded that VDR and its functional polymorphisms may play an important role in the pathogenesis of asthma

Non-association of IL-12 +1188 and IFN-gamma +874 polymorphisms with cytokines serum level in occult HBV infected patients

Occult hepatitis B infection [OBI] is identified as a form of hepatitis in which despite the absence of detectable HBsAg, HBV-DNA is observed in peripheral blood of patients. The main aim of this study has been to investigate the association between polymorphisms in +874 of IFN-gamma and +1188 of IL-12 with their serum level in patients suffering from OBI. In this experimental study, plasma samples of 3700 blood donors were tested for the presence of hepatitis B surface antigen [HBsAg] and anti-HBc by ELISA. The HBsAg[-]/anti-HBc[+] samples were selected and screened for HBV-DNA by PCR. HBV-DNA positive samples were assigned as OBI cases and ARMS-PCR techniques were performed to examine the two known polymorphisms within IL-12 and IFN-gamma. In addition, the serum levels of IL-12 and IFN-gamma were also determined by ELISA. Results of this study demonstrated that, 352 [9.5%] out of 3700 blood samples were HBsAg[-]/anti-HBc[+]and HBV-DNA was detected in 57/352 [16.1%] of HBsAg[-]/anti-HBc[+] samples. Our results showed that groups showed significant difference in CC allele of +1188 region of IL-12 and no difference was observed in the other evaluated genes. Our results also showed that the alleles of +1188 region of IL-12 and alleles of +874 of IFN-gamma were also not associated with serum level of cytokines. According to the results of this study, it may be concluded that the polymorphisms in +1188 region of IL-12 and +874 region of IFN-gamma would not affect the expression of both cytokines at serum level in OBI patients

Effect of shark liver oil on peritoneal murine macrophages in responses to killed-Candida albicans

Shark Liver Oil [SLO] is an immunomodulator. Macrophages play a key role in host defense against pathogens like fungi. Candida albicans have mechanisms to escape immune system. We determined the effect of killed-Candida on the in vitro viability of macrophages and the effect of SLO on augmentation of this potency. Peritoneal macrophages were separated and cultured [3-105/well]. At first, the effect of killed-Candida [200 cells/well] on macrophage viability was evaluated, using MTT test. Then, MTT was performed on macrophages stimulated with killed-Candida in the presence of SLO. Killed-Candida suppressed the ability of MTT reduction and hence macrophages viability [P=0.026], but addition of SLO [100 mg/ml] significantly enhanced cell viability [P=0.00]. So, SLO could neutralize the inhibitory effect of Candida. Simultaneous with cytotoxic effect of killed-Candida cells on macrophages viability, SLO augment macrophages viability. So, it can be applied in candidiasis as a complement

Effect of cell wall, cytoplasmic fraction and killed-Candida albicans on nitric oxide production by peritoneal macrophages from BALB/c mice

The fractions of Candida albicans have been used as an immunomodulator. The present work assessed the effect of different fractions of C. albicans on nitric oxide [NO] production by mice peritoneal macrophages. Cell wall and cytoplasmic fractions of C. albicans ATCC 10321 strain were extracted. Mice peritoneal macrophages were purified and cultured. Different concentrations of both fractions and also killed C. albicans cells were used for macrophages stimulation and evaluation of NO production. NO amount was detected in culture supernatants of macrophages by Griess reagent. Also, MTT assay was performed to assess the viability of macrophages. The results elucidated that suppressive effect of cell wall proteins on NO release was significant at the dose of 100 micro g/ml [P=0.01], while cytoplasmic fraction increased NO amount at the dose of 1 micro g/ml compared to the control group [P=0.003]. Augmentation of NO production was statistically significant at 200 killed C. albicans per well [P=0.006]. According to our findings, cytoplasmic fractions and killed C. albicans have a positive effect on NO production by peritoneal macrophages, while cell wall fractions did not. Therefore, it is proposed that C. albicans fractions can be studied more as inflammation modulators

Evaluation of relation between IL-4 and IFN-gamma polymorphisms and type 2 diabetes

Although, type 2 diabetes is the most frequent type of diabetes, its main cause is yet to be clarified. Several environmental and genetic parameters are believed to be involved in diabetes. It has also been established that cytokines play key roles in pathogenesis of diabetes. Expression of cytokines is different from person to person and in different societies. Several studies showed that polymorphisms of +874 of interferon-gamma [IFN-gamma] and -590 of interleukin-4 [IL-4] are associated with the regulation of expression of these genes. This study was aimed to find polymorphisms of these regions in type 2 diabetes patients. In this experimental study peripheral blood samples were collected from 160 type 2 diabetic patients and 160 healthy controls. DNA was extracted by salting out method. Polymorphisms of +874 of 1FN-gamma and -590 of IL-4 were analyzed by ARMS-PCR and RFLP-PCR. Our findings indicated that TT genotype of IFN-gamma was increased in type 2 diabetic patients compared to the control but difference was not significant. Our results didn't show any significant difference between IL-4 genotype in diabetic and healthy controls either. Our results suggested that TT genotype of IFN-gamma can be associated with diabetes. This association can be described by the fact that over expression of IFN-gamma shifts immune system to Th 1; therefore, pancreatic cells can be miscarried by immune cells