Systemic Th17 response in the presence of periodontal inflammation

Abstract The relationship between periodontitis and the pathogenesis of other inflammatory diseases, such as diabetes, rheumatoid arthritis and obesity has been an important topic of study in recent decades. The Th17 pathway plays a significant role in how local inflammation can influence systemic inflammation in the absence of systemic pathology. Objective: To determine Th17 biased-cells in systemically healthy patients in the presence of generalized chronic periodontitis. Methodology: A total of 28 patients were recruited without systemic inflammatory pathology, which was determined by clinical history, the Health Assessment Questionnaire (HAQ) and rheumatoid factor detection. Of these patients, 13 were diagnosed as healthy/gingivitis (H/G) and 15 as generalized chronic periodontitis (GCP). Th17 (CD4+CD161+) cells and Th17IL23R+ (CD4+CD161+IL-23R+) cells were quantified by flow cytometry, based on the total cells and on the lymphocyte region, termed the "enriched population" (50,000 events for each). Results: The percentages of Th17 cells of the H/G and periodontitis groups were similar on total cells and enriched population (19 vs 21.8; p=4.134 and 19.6 vs 21.8; p=0.55). However, Th17IL23R+ cells differ significantly between periodontally healthy patients and generalized chronic periodontitis patients in both total cell (0.22% vs 0.65%; p=0.0004) and enriched populations (0.2% vs 0.75%; p=0.0266). Conclusions: GCP patients (otherwise systemically healthy) were characterized by increased Th17-proinflammatory cell phenotype positive for the IL-23 receptor in peripheral blood. The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis.

[Evaluation of cytokines changes in patients infected with giardia lamblia in comparison with healthy subjects]

Human Giardisis infection is caused by the flagellate protozoa. Giardia lamblia, which lives in the small intestine, causing damage and may also cause gastrointestinal symptoms. This parasitic disease has a worldwide distribution and prevalence varies from 5% to 30%. The role of both humeral and cellular immune response in the host defense against parasites has proven. Since an immune response is directly affected by cytokine, study of cytokines changes in patients with giardiosis is of particular importance. In this study the serum levels of IL-2 - 4 - 6 to 17 and 23 in patients and healthy subjects were measured and compared. Fasting blood samples were taken from the volunteers, ELISA was performed to measure cytokines. In this study, the amount of IL-2 and IL-6 in infected patients was significantly more than the controls, but IL-4 levels were significantly lower in infected individuals [P=0.0001]. Also for the first time in people with giardiasis IL- 17 and IL-23 was measured and there was a significant aifference in these cytokines between the infected patients healthy controls[respectively P=0.044 and P=0.03]. Host defense response against parasitic infections, is directly and affected by cytokines. Increased interleukin 2, 6, 17 and 23 in patients with Giardiosis was probably caused by immune response and local intestinal inflammation

relation between the level of interleukin-23 with duration and severity of ulcerative colitis

In this study, we determined the relationship between the serum level of IL-23 and the severity of ulcerative colitis [UC] among our population. A recent major breakthrough for describing the pathogenesis of intestinal tissue injury in inflammatory bowel disease [IBD] is the pathway related to interleukin-23 [IL-23]. We performed a prospective case-control study on a total of 85 new patients with ulcerative colitis, recruited from a general referral hospital. Forty ethnically matched healthy controls were also enrolled among hospital staffs and analyzed. Serum IL-23 level was quantified using an electrochemiluminescence immunoassay [ECLIA] method with an immunoassay analyzer. The mean serum IL-23 level in the group with ulcerative colitis was significantly higher than the healthy individuals [347.5 +/- 130.9 pg/ml versus 233.5 +/- 86.3 pg/ml; p<0.001]. There was a positive correlation between the serum level of IL-23 and disease duration [r = 0.27, p = 0.04]. Also, a direct relationship was found between the serum level of IL-23 and the severity of disease [mean IL-23 in mild UC = 296.2 +/- 51.2 pg/ml; in moderate UC = 356.1 +/- 142.9 pg/ml; and in severe UC=399.3 +/- 163.8 pg/ml, p=0.04]. Serum level of IL-23 is directly correlated with the duration and severity of ulcerative colitis

Reduced interleukin-17 expression of Burkholderia pseudomallei-infected peripheral blood mononuclear cells of diabetic patients.

Burkholderia pseudomallei is the causative agent of melioidosis. One of the main risk factors for B. pseudomallei infection in endemic areas is diabetes mellitus. The present study investigated IL-17 mRNA and protein expression by peripheral blood mononuclear cells in response to B. pseudomallei infection in 10 diabetic patients in comparison to 10 healthy blood donors. The IL-17 expression in diabetic patients was significantly lower (p < 0.05) than in the controls. However, IL-23 mRNA expression of the 2 groups was comparable. The present findings suggest that melioidosis affects T cell IL-17 production and that patients with diabetes mellitus have a defective IL-17 production in response to this type of infection.