CD4+ T cell responses are critical for the pathogenesis of Helicobacter pylori infection. The present study evaluated the role of the Th17 subset in H. pylori infection. H. pylori infection induced significant expression of IL-17 and IFN-g in mouse gastric tissue. IL-23 and IL-12 were increased in the gastric tissue and in H. pylori-stimulated macrophages. Cell responses were examined by intracellular staining for IFN-g, IL-4, and IL-17. Mice infected with H. pylori developed a mixed Th17/Th1 response; Th17 responses preceded Th1 responses. Treatment of mice with an anti-IL-17 Ab but not a control Ab significantly reduced the H. pylori burden and inflammation in the stomach. H. pylori colonization and gastric inflammation were also lower in IL-17 2/2 mice. Furthermore, administration of recombinant adenovirus encoding mouse IL-17 increased both H. pylori load and inflammation. Further analysis showed that the Th1 cell responses to H. pylori were downregulated when IL-17 is deficient. These results together suggest that H. pylori infection induces a mixed Th17/Th1 cell response and the Th17/IL-17 pathway modulates Th1 cell responses and contributes to pathology. The Journal of Immunology, 2010, 184: 5121-5129. H elicobacter pylori is a Gram-negative, microaerophilic bacterium that resides extracellularly in the gastric mucosa and infects .50% of the population worldwide. H. pyloriinduced chronic inflammation is the cause of gastritis and peptic ulcers and a risk factor for gastric cancer (1, 2). H. pylori infection causes severe local inflammation in the gastric mucosa. CD3 + CD4 + T cells are increased in infected gastric lamina propria and play important roles in the pathogenesis of persistent H. pylori infection (3). Traditionally, CD4 + T cells are classified into two main classes: Th1 and Th2, on the basis of their cytokine secretion and immune regulatory function. Th1 cells secrete IFN-g, IL-2, and IL-12 and regulate cellular immunity, whereas Th2 cells produce IL-4, IL-5, and IL-13 and mediate humoral responses. To date, studies of immune responses to H. pylori have largely focused on Th1 and Th2 cells, and it is generally accepted that H. pylori infection results in a Th1-dominant response and that gastric inflammation largely depends on Th1 cell responses (3-6); however, IFN-g secretion alone is insufficient to induce gastritis (3). Thus, the detailed mechanism of pathogenesis is not clear. A novel subset of effector T cells, identified by secretion of IL-17, has been defined as Th17 cells. Th17 cells are distinct from Th1 and Th2 cells in their differentiation and function (7,8). TGF-b and IL-6 from activated macrophages/dendritic cells are required for Th17 cell differentiation in murine systems (9), whereas IL-12 and IFN-g promote Th1 cell development and IL-4 primes Th2 cell differentiation. The expansion and survival of Th17 cells are promoted by IL-23 (9), a heterodimeric cytokine composed of a unique p19 subunit and a p40 subunit shared with IL-12 (10). The identification of Th17 cells necessit...

No abstract

No abstract

No abstract

This study aimed to assess the effects of different anthropometric indices and their changes on the risk of incident dyslipidemia among the Chinese population. From the Guizhou population health cohort study, 2989 Chinese adults without dyslipidemia at baseline were followed up. Anthropometric parameters including waist circumference (WC), body mass index (BMI), waist-to-height ratio (WHtR), and their changes in the latter two indices, and serum lipids were tested after at least 8 h fasting. Hazard ratio (HR), adjusted hazard ratio (aHR), and 95% confidential interval (CI) were calculated to estimate the association between anthropometric parameters and dyslipidemia risk using multivariate Cox regression. A total of 2089 (69.98%) new dyslipidemia cases were identified over an average follow-up of 7.0 years. Baseline BMI (aHR = 1.12, 95%CI 1.01, 1.23) and WHtR (aHR = 1.06, 95%CI 1.00, 1.13) were positively associated with higher risks of incident dyslipidemia but not WC. Each 5.0 kg/m2 increment of BMI or 0.05-unit increment of WHtR was significantly associated with 43% or 25% increased risk of incident dyslipidemia, respectively. The aHRs (95%CI) of incident dyslipidemia for subjects maintaining or developing general obesity were 2.19 (1.53, 3.12) or 1.46 (1.22, 1.75), and 1.54 (1.23, 1.82) or 1.30 (1.06, 1.60) for subjects maintaining or developing abdominal obesity, respectively. Linear trends for aHRs of BMI, WHtR change, and BMI change were observed (p for trend: 0.021, <0.001, <0.001, respectively). BMI, WHtR, and their changes were closely associated with the incidence of dyslipidemia for Chinese adults. Loss in BMI and WHtR had protective effects on incident dyslipidemia, whereas gain of BMI or WHtR increased the dyslipidemia risk. Interventions to control or reduce BMI and WHtR to the normal range are important for the early prevention of dyslipidemia, especially for participants aged 40 years or above, male participants, and urban residents with poor control of obesity.

No abstract

No abstract

No abstract