Vitamin D levels vary during antiviral treatment but are unable to predict treatment outcome in HCV genotype 1 infected patients.

Background: Different parameters have been determined for prediction of treatment outcome in hepatitis c virus genotype 1 infected patients undergoing pegylated interferon, ribavirin combination therapy. Results on the importance of vitamin D levels are conflicting. In the present study, a comprehensive analysis of vitamin D levels before and during therapy together with single nucleotide polymorphisms involved in vitamin D metabolism in the context of other known treatment predictors has been performed.

Improved responses to pegylated interferon alfa-2b and ribavirin by individualizing treatment for 24-72 weeks.

Background & Aims: Guidelines recommend that patients with chronic hepatitis C virus (HCV) infection be treated with pegylated interferon and ribavirin for 24, 48, or 72 weeks, based on their virologic response to treatment. We investigated the effects of treating patients for individualized durations.

Methods: We treated 398 treatment-naïve patients who had HCV genotype 1 infections with pegylated interferon alfa-2b and ribavirin for 24, 30, 36, 42, 48, 60, or 72 weeks (mean of 39 weeks, termed individualized therapy); the duration of therapy was determined based on baseline viral load and the time point at which HCV RNA levels became undetectable (measured at weeks 4, 6, 8, 12, 24, and 30).

Toll-like receptor-dependent activation of antigen-presenting cells affects adaptive immunity to Helicobacter pylori.

Background & Aims: Recognition of infection leads to induction of adaptive immunity through activation of antigen-presenting cells (APCs). Among APCs, dendritic cells (DCs) have the unique capacity to deliver antigens from the periphery to T cells in secondary lymphoid organs.

Methods: We analyzed molecular mechanisms of the Helicobacter pylori-induced APC activation in vitro and investigated the influence of Myd88 signaling on the phenotype of adaptive immunity to H pylori in a murine infection model.

H pylori and gastric cancer: shifting the global burden.

Infection with H pylori leads to a persistent chronic inflammation of the gastric mucosa, thereby increasing the risk of distal gastric adenocarcinoma. Numerous studies have determined a clear correlation between H pylori infection and the risk of gastric cancer; however, general eradication is not recommended as cancer prophylaxis and time points for treatment remain controversial in different areas of the world. Prevalence rates in Western countries are decreasing, especially in younger people (< 10%); and a decline in distal gastric adenocarcinoma has been observed.

CD25+/Foxp3+ T cells regulate gastric inflammation and Helicobacter pylori colonization in vivo.

Background & Aims: Helicobacter pylori infects more than half of the world's population. In contrast to most other pathogens, the microbe persists for the virtual life of its host. It is unclear why the immune system is unable to eliminate the infection, but recent studies suggested that CD4+/CD25+/Foxp3+ regulatory T cells may be involved in this process.

VacA-associated inhibition of T-cell function: reviewed and reconsidered.

Chronic Helicobacter pylori infection is characterized by dense infiltration of the mucosa with neutrophilic granulocytes, lymphocytes, and monocytes/macrophages. Among these different cell types, T-lymphocytes are the most intriguing and crucial cells for the elimination of the bacteria. Previous studies have elucidated possible mechanisms on how bacteria could interfere with the human immune response and claimed that especially the secreted vacuolating toxin VacA may be responsible for the chronic persistence of the bacteria.

Human dendritic cells respond to Helicobacter pylori, promoting NK cell and Th1-effector responses in vitro.

Helicobacter pylori infection leads to chronic gastric inflammation. The current study determined the response of human APCs, NK cells, and T cells toward the bacteria in vitro. Human monocyte-derived dendritic cells (DC) were incubated with bacteria for 48 h.