pylori infection and insulin resistance measured by a quantitative homeostatic model. A potential association was

found, and the interesting points to highlight being that impaired ghrelin production and low levels of leptin in patients with H. pylori infection induce elevated fasting insulin levels in insulin-resistant patients and impaired insulin sensitivity, respectively. In an interesting Brazilian study of Silva et al. [43], the authors evaluated the association between the presence of H. pylori in the liver biopsy specimens determined by PCR and the etiology and stage of hepatic disease and the cytokine pattern (ELISA) displayed 3-MA price by the patients. This prospective study was carried out on 147 patients (106 pts with primary hepatic diseases and 41 with metastatic tumors) and 20 liver donors as controls. According to the results

of this study, the detection of H. pylori DNA in the liver was independently associated with hepatitis B virus/hepatitis C virus, liver metastases of pancreatic carcinoma. The cytokine pattern was characterized by high IL-10, low or absent IFN-γ, and decreased IL-17A levels (p < .001). In addition, the bacterial DNA was never detected in the liver of patients with alcoholic see more cirrhosis and autoimmune hepatitis that are associated with Th1/Th17 polarization. It is important to stress that gastric H. pylori status, as evaluated by ELISA and/or UBT, was positive in 78.9% of patients and in 55% of control liver donors. Taking into account that H. pylori-positive serology/UBT status was independently associated with the presence of H. pylori DNA in the liver and strains isolated from the liver had similar characteristics to those isolated from the stomach, the authors hypothesize that gastric H. pylori can reach the liver by retrograde transfer from the duodenum when cytokine pattern of the host is more regulatory type than proinflammatory find more type. However, according to the results of this study the regulatory cytokine profile, characterized by IL-10,

was detected in a certain number of patients with gastric H. pylori infection, but without evidence of H. pylori in the liver. However, the host immune response may represent the ability of the liver in clearing certain microorganism, thus reflecting the possibility that the presence of H. pylori could be more a consequence rather than a cause of hepatic diseases. Le Roux-Goglin et al. [44] hypothesized that, under pathologic conditions in vivo, hepatocytes can also assemble podosomes, peculiar dot-like structures made of actin and containing adhesion structures, such as vinculin, integrins, signaling proteins, and membrane-type 1 matrix metalloproteinase. This study for the first time showed that mouse hepatocytes infection with four strains of H. pylori that were tested doubled the number of podosome forming cells in vitro, suggesting a common pathogenic mechanism to different strains.