Background Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders of the gastrointestinal tract. It is fundamentally related to a dysregulated immune response in the intestinal mucosa against microbiota in genetically predisposed individuals. Among the genetic and immunological factors that are suggested to have role in etiology and pathogenesis of IBD are human leukocyte antigen (HLA)-G molecules. Therefore, soluble HLA-G (sHLA-G) serum level and genetic association with HLA-G 14-bp insertion (Ins)/deletion (Del) polymorphism was analyzed in 100 IBD patients; 50 ulcerative colitis (UC) and 50 Crohn’s disease (CD), and 100 controls. Results sHLA-G level was significantly elevated in IBD patients compared to controls (174.7 ± 27.1 vs. 126.8 ± 15.1; corrected probability [pc] < 0.001). The level was also elevated in UC patients compared to CD patients but the difference was not significant (180.5 ± 27.1 vs. 168.9 ± 26.3; p = 0.059). Receiver operating characteristic analysis confirmed the significance of sHLA-G in total IBD, UC, and CD patients (area under curve = 0.944, 0.961, and 0.927, respectively). The genetic association was analyzed under five genetic models (allele, recessive, dominant, overdominant, and codominant). At the allele level, Del allele frequency was significantly increased in total IBD patients (Odds ratio [OR] = 1.93; 95% confidence interval [CI] = 1.27–2.94; pc = 0.018) and CD patients (OR = 2.08; 95% CI = 1.23–3.54; pc = 0.042) compared to controls. Among UC patients, a similar increased frequency was observed, but the pc value was not significance (OR = 1.79; 95% CI = 1.07–3.00; p = 0.031). At the genotypic level, Del/Del genotype was associated with a significantly increased IBD-risk in total patients under codominant model (OR = 4.06; 95% CI = 1.56–10.56; pc = 0.024). sHLA-G level was not influenced by the Ins/Del polymorphism. Conclusions This study demonstrated a significant increase in serum level of sHLA-G in UC and CD patients. Further, HLA-G 14-bp Ins/Del polymorphism may be associated with susceptibility to IBD, particularly CD.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder,  the etiology and pathogenesis of which have been suggested to be influenced by cytokines. Two main clinical types of IBD are recognized, namely ulcerative colitis (UC) and Crohn's disease (CD). The present study examined serum levels of two cytokines (IL-17A and IL-23) in 60 IBD patients (30 UC and 30 CD) and 30 healthy controls. The levels were correlated with age, gender, cigarette-smoking status, disease duration, family history, disease extension, symptoms, extra-intestinal manifestations, and medication. The results depicted that IL-17A level was significantly higher in UC and CD patients compared to control (45.2 ± 23.3 and 47.5 ± 34.4 vs. 15.6 ± 7.5 pg/ml, respectively; p < 0.001). Serum level of IL-23 was similarly increased in UC and CD patients compared to control (64.1± 23.7 and 62.5 ± 27.3 vs. 25.2 ± 11.1 pg/ml, respectively). However, the level of both cytokines showed no significant variation between UC and CD patients (p = 0.713 and 0.777, respectively). Distributing UC and CD patients into subgroups according to some characteristics revealed that IL-17A level was significantly increased in UC male compared to female patients (57.3 ± 18.2 vs. 34.5 ± 22.5 pg/ml; p = 0.005). It was also significantly increased in smoker UC patients compared with non-smoker patients (51.9 ± 19.4 vs. 31.6 ± 25.5 pg/ml; p = 0.022). Smoker CD patients also showed a significantly increased level of IL-23 compared to non-smoker patients (72.7 ± 28.5 vs. 52.2 ± 22.6 pg/ml; p = 0.038). In the case of family history, IL-23 level was significantly decreased in UC patients with a family history of IBD compared to CD patients with a family history (84.5 ± 24.3 vs. 50.4 ± 17.0 pg/ml.; p = 0.042). In conclusion, the present data suggest a role for IL-17A and IL-23 in the etiology and pathogenesis of UC and CD.

Background Human leukocyte antigen-G (HLA-G) has been proposed to influence susceptibility to inflammatory bowel disease (IBD). Therefore, the genetic association between HLA-G alleles and two clinical phenotypes of IBD (ulcerative colitis [UC] and Crohn’s disease [CD]) was evaluated in Iraqi patients. A case-control study was performed on 50 UC and 50 CD patients and 100 healthy controls (HC). Three HLA-G alleles (G*01:03, G*01:04, and G*01:05N) were determined using sequence-specific polymerase chain reaction assay followed by product digestion with restriction endonucleases (Hinf-I, BseR-I, and PpuM-I, respectively). Results The G*01:03 allele was not detected in IBD patients (UC and CD) or HC, while G*01:04 and G*01:05N alleles showed polymorphic frequencies. The allele G*01:04 was significantly associated with susceptibility to UC (odds ratio [OR] = 2.55; 95% confidence interval [CI] = 1.27–5.13; corrected probability [pc] = 0.018) and CD (OR = 4.45; 95% CI = 2.11–9.41; pc < 0.001). The allele G*01:05N was also associated with increased risk of UC (OR = 4.17; 95% CI = 1.32–13.21; pc = 0.032) and CD (OR = 4.75; 95% CI = 1.53–14.78; pc = 0.014). These associations were more pronounced in IBD (UC + CD), and a significantly increased risk for IBD was found with the alleles G*01:04 (OR = 3.32; 95% CI = 1.86–5.95; pc < 0.001) and G*01:05N (OR = 4.46; 95% CI = 1.59–12.47; pc = 0.008). A stratification of IBD patients according to some demographic and clinical characteristics revealed that frequencies of both alleles showed no significant differences between the subgroups of patients in each stratum. Soluble HLA-G was not influenced by HLA-G alleles in patients or HC. UC was an exception, and the presence of G*01:04 allele was associated with a significantly higher mean of soluble HLA-G compared to patients without the allele (189.6 ± 24.0 vs. 168.6 ± 27.2 ng/mL; p = 0.033). Conclusion This study indicated that HLA-G*01:04 and HLA-G*01:05N alleles may influence susceptibility to UC and CD in Iraqi patients.

Background: The live microorganisms that present in food in addition dietary supplements called Probiotics they have beneficial effect in the human intestine. In the last years, Probiotics has become within treatment options for several disease included immune system. The advent and use of probiotics seem to be increasing day by day all over the world. Objective: The current study included detection of efficacy Pediococcus acidilactici as immunomodulatory in mice that treated with cyclophosphamide. Design: To detect efficacy of Pediococcus acidilactici as immunosuppressive model was used. This model was completed by taking 20 male BALB/C mice with six-weeks old to divide into (5) groups :(G 1) group is the normal control. (G2) group: the group that injected with cyclophosphamide. (G3) group: the immunosuppression plus Pediococcus acidilactici (6×108 CFU/ml). (G4) group: the immunosuppression plus Pediococcus acidilactici (6×104 CFU/ml). last (G5) group : is the group that treated with probiotics. Results: In the current study, thymus and spleen indicators were significantly higher in treated groups than those of (G1) group (NC) with (0.323±0.34) (P<0.05), also Macrophages phagocytosis showed a clear increase in the three treated groups (76.625±108, 72.125±1.65, 87.750±1.32) respectively with significantly (P<0.05), as a compared with (G1) group (NC). Conclusions: The current study reveals the ability of Pediococcus acidilactici (6×109) CFU/ml to accelerate the healing of cyclophosphamide immunosuppressive mice. So, the activity role of probiotic strain as immunomodulator in this study leads us to urge the use it as an alternative treatment for chemical drugs that used against immunosuppression.

Objective: The present study was conducted to investigate the effects of Artemisia extract on some immunological parameters in streptozotocin-induced diabetic mice. Methods: After preparation of Artemisia extract, many chemical tests were used to identify the type of element and compounds presented in this plant using many chemical techniques. Thirty five streptozocin (STZ) induced diabetes mice were divided in to 5 groups; the first group provided only with water, the other four groups were consumed orally ingested the plant extract in four different concentration (2000, 1000, 500,250) mg/Kg of body weight. Another 10 mice didn’t injected with STZ were divided in to two groups; one consumed Artemisia (Art group), and the second consumed only normal saline (Cont. group). After 14 days of diabetes induction and Artemisia extract treatment, the mice were sacrificed. Blood and tissue (brain, spleen and kidney) were collected. Fasting blood sugar and insulin levels were determine in the serum. Furthermore Tumor Necrosis Factor- alpha (TNF- α) and Interleukin-6 (IL-6) levels were determined in the serum and aliquots of homogenize tissues. Results: Results declared that the extract of Artemisia fruit contains high levels of active compounds especially antioxidant compounds. IL-6 and TNF-α levels were decreased while insulin and glucose levels were increased in the STZ- induce mice group. Artemisia extract effects differently on glucose and insulin levels depend on its concentration. Interestingly, IL-6 and TNF-α levels increase in serum, brain and spleen of the STZ-induce mice group consumed different concentration of Artemisia but it normalized in the STZ-induce mice group consumed 250 mg/kg Artemisia, as well as insulin and glucose levels for the same group, while there was no difference in kidney. Conclusion: Artemisia can control diabetes in 1000 and 500mg/Kg through controlling insulin level, and in the other hand, using the plant extract in 250mg/Kg ,acts as immune modulator for anti-inflammatory agents IL-6 and TNF-α.