Glycyrrhizin down-regulates CCL2 and CXCL2 expression in cerulein-stimulated pancreatic acinar cells.

Many inflammatory chemokines release from leukocytes and pancreatic acinar cells which play important roles in pathophysiology of acute pancreatitis (AP). Of interests, CXCL2 and CCL2 have been shown elevated in the plasma of patients with AP. We have recently found that Glycyrrhizin (GZ) attenuates AP in mice model. In this study, we aimed to investigate the direct effect of GZ on expression levels of CCL2 and CXCl2 in isolated pancreatic acinar cells. Isolated acinar cells were isolated from the pancreas of healthy C57BL/6 mice, stimulated with cerulein (10(-7) M) and then treated with either PBS or different doses of GZ. The levels of CCL2 and CXCL2 expression at mRNA were assessed by qRT-PCR. Conditioned media from supernatants of each cells culture condition were collected for detection of CCL2 and CXCL2 levels by ELISA. First, we observed that cerulein significantly upregulates both cytokines expression in acinar cells. Moreover, we treated the acinar cells with GZ and found that GZ significantly downregulates CCL2 and CXCL2 expression at mRNA levels in a dose-dependent manner. Consistently, the conditioned media of GZ-treated cells contained a significant lower levels of CCL2 and CXCL2 (p<0.05). In conclusion, our data demonstrate for the first time that GZ directly downregulates CCL2 and CXCL2 levels in cerulein-stimulated acinar cells which may explain the mechanism of therapeutic effects of GZ in cerulein-induced AP in mice.

Breastfeeding and Helicobacter pylori Infection in Early Childhood: a Continuing Dilemma.

OBJECTIVE: Helicobacter pylori (H. pylori) is the most common chronic bacterial infection in humans. Chronic colonization increases the risk of duodenal ulcer and gastric cancer. The risk factors for acquiring the infection have been extensively studied. However, there are conflicting results on the role of breastfeeding in the prevention of H. pylori infection. We conducted a study to evaluate the effects of breastfeeding on the H. Pylori infection in Kurdish children in Sanandaj, IR Iran. METHODS: A historical cohort study was carried out from January 2011 through December 2012. Totally 221 children who were going to attain 2 years old during the study period were randomly enrolled. They were divided into two groups, i.e. breastfed and non-breastfed. We used H. pylori stool antigen test to detect infection in the selected group of children after age of 2 years and cessation of breastfeeding. Each group was subdivided into two subgroups, infected and non-infected. The associations of breastfeeding with H. pylori infection was assessed using statistical software. FINDINGS: We found no difference in the odds of infection between breastfed and non-breastfed groups (OR=0.809, 95% CI [0.453-1.444]). An association between age and the prevalence of infection was found (P=0.008). There was an increase in the odds of infection as the family size grew (OR=1.93, 95% CI [1.04-3.6]) as well as increasing housing density (OR=2.12, 95% CI [1.10-4.10]). CONCLUSION: The data suggests that breastfeeding in infancy does not protect against H. pylori infection for long duration among studied children in Iran. The protective effects of breastfeeding, if any, are at most transient.