Background- Escherichia coli Serogroup O157:H7 (E. coli O157:H7) is a zoonotic bacterial pathogen that causes symptoms ranging from self-limiting bloody diarrhea to severe hemorrhagic colitis in humans. E. coli O157:H7 infection can also cause extra-intestinal illness, most importantly hemolytic-uremic syndrome (HUS). The aims of this study was to evaluate the effect of two types of E. coli possess O157:H7 antigen and E. coli possess O157:H7:K99 antigen on humoral and cellular immunity in mice. Materials and Methods- Three groups of mice (twenty in each) were used, first group was immunized twice at two weeks intervals subcutaneously (S/C) with 0.5 ml of heat killed E. coli O157:H7 (first vaccine) containing 1×108 C.F.U, second group immunized similarly with heat killed E. coli possess O157:H7+K99 (second vaccine), third group was injected S/C with phosphate buffer saline (PBS). Blood samples were collected at 2, 4 and 6 weeks post booster dose. Humoral immunity was detected by ELISA test, while cellular immunity detected by delayed type hypersensitivity test (DTH-skin test). Post six weeks of vaccination, the immunized and control mice groups were challenged with (1×1010) of virulent E. coli. Results- Antibody titers (IgG) was increased significantly (p<0.05) at 2,4 and 6 weeks in the immunized group and the maximum increase was determined at fourth week [O157 vaccine (751.5±21.5)] & [K99+O157:H7 vaccine (802.8±1.85)] in comparison with the control group which remained within the normal value in all times of the experiment. In DTH test, immunized groups showed a significant increase in footpad thickness after 24&48 hours post inoculation with soluble antigen in comparison with control group. A significant protection was observed in immunized groups challenged with 4LD50 (4 ×1010 cells) compared with control group of mice which died within 1-3 days. Conclusion- Immunization of mice with different E. coli vaccines was induced humoral and cellular immune responses against challenge with virulent E. coli. These vaccines of E. coli [O157:H7:K99] and [O157:H7] vaccine proved efficacy in inducing immunity.

Fenvalerate is a synthetic pyrethroid commonly used in agriculture and other domestic applications. The present work studied the effect of vitamin E on immunotoxicity of fenvalerate in albino rats. Treating animals with fenvalerate (1/10 LD50, 3 times weekly for 2 weeks) caused obvious histopathological alterations in the thymus represented by depletion of cortical thymocytes, atrophy of medulla, hemorrhages in the stroma and focal areas of necrosis. Hematological results showed an increase in the total leucocytes, in the percentage of lymphocytes and a significant decrease in percentages of monocytes and neutrophilis. Biochemical results revealed an increase in MDA and a decrease in the activity of SOD and CAT. Treating mice with fenvalerate and vitamin E (20mg/kg body weight) improved the architecture of the thymus. The thymus showed an increase in the cellularity and the number of leukocytes becomes nearly to the normal value. Moreover, the activity of SOD and CAT was enhanced and lipid peroxidation was diminished. These effects are attributed to the antioxidant activity of vitamin E.

Background: There is growing evidence that genetic aspects play a role in the onset and severity of periodontitis. However; numerous studies have pointed to the contribution of the human leukocyte antigens (HLA)/alleles as a potential genetic factor in aetiopathogenesis of periodontitis. Aims of Study: This study was performed to investigate the association of human leukocyte antigens class II genetypes (HLA-DRB1) and the susceptibility to chronic periodontitis in Iraqi patients. Materials and Methods: Thirty subjects with chronic periodontitis and 20 apparently healthy volunteers participated in this study. Blood samples were collected from patients and controls, DNA was extracted from blood samples, and then HLA-RDB1 genotyping was performed by polymerase chain reaction-specific oligonucleotide probes (PCR-SSO) method. Results: The present data revealed that the frequencies of HLA-DRB1*03 and HLA-DRB1*11 alleles were significantly higher in patients than in healthy controls (P= 0.004 and P=0.006 respectively), on the other hand low frequency of HLA-DRB1*04 allele was found in patients when compared with healthy control (P= 0.020). However, there is no association between the frequency of these specific HLA-alleles and patients with positive family history. Conclusion: This study demonstrates that HLA-DRB1*03 and HLA-DRB1*11 alleles may contribute to the increased susceptibility to chronic periodontitis. While HLA-DRB1*04 allele may confer protective effects against this disease.

Previous studies have reported that ligands of the aryl-hydrocarbon receptor (AhR) can influence the induction of different autoimmune diseases by altering the development of IL-17+ CD4+ Th17 cells or Foxp3+ CD4+ Treg cells. CD8+ T cells are also involved in mediating or regulating autoimmune destruction, and are known to polarize into different subsets. However, the effects of AhR-ligands on CD8+ T cell phenotypes and effector functions have not yet been investigated. In the present research, the effects of specific AhR-ligands, and the ligand precursor, tryptophan, on CD8+ T cell mediated autoimmunity were investigated for the first time using the RIP-LCMV-GP transgenic diabetes model. We find that, the co-injection of tryptophan, curcumin, or quercetin together with immunization with mature bone marrow- derived dendritic cells carrying self-antigen, increased the incidence of diabetes induced in RIP-GP/P14 TCR transgenic mice. In contrast, co-injection with the AhR-ligands FICZ and I3C failed to stimulate diabetes. The activation of diabetes following injection of tryptophan, curcumin, or quercetin, correlated with their ability to increase IL-17+CD8+ (Tc17) and IFN-γ+CD8+ (Tc1) cell populations, in vivo. Furthermore, in vitro experiments showed that tryptophan, curcumin, or quercetin treatments directly promoted significantly increased Tc1 and Tc17 cell development, whereas FICZ and I3C treatments directly promoted IL-10+CD8+ T cell development while having no significant effect on either Tc1 or Tc17 subsets. These novel findings indicate that some AhR-ligands can increase CD8+ T cell-mediated autoimmune responses by skewing T cell polarization towards effector subsets.

IL-17-producing Th cell subsets (Th17) are thought to be involved in autoimmune disease pathogenesis. The aryl-hydrocarbon receptor (AhR) is highly expressed in Th17 cells and AhR-ligands can skew T cell polarization towards either a Th17 or Treg phenotype. Previous studies have reported effects of AhR-ligands on experimental autoimmune encephalomyelitis. However, the ability of AhR-ligands to influence other autoimmune diseases has not been investigated. Here we show that mice lacking the cytokine receptor subunit gp130 on T cells, which have amplified Treg and reduced Th17 cell development, are protected from multiple low doses of streptozotocin (MLD-STZ)-induced diabetes. Furthermore, we find that the AhR-ligands including; curcumin, quercetin, and tryptophan, significantly increase the incidence of diabetes in C57Bl/6J mice after sub-diabetogenic doses of STZ. Enhanced autoimmune activation correlated with increased Th17 and Th1 populations, whereas no significant effect was noticed on Foxp3+ Treg cells following the AhR-ligand administration. In contrast, the AhR-ligands FICZ and I3C decreased the incidence of diabetes, which correlated with a significant increase in Treg cells. Our findings demonstrate a T cell gp130-dependent pathway required for cell-damage-induced diabetes, and reveal the ability of different AhR-ligands to modulate autoimmunity based on their ability to alter the balance of Th17/Treg subsets.