K Miu1, L Sun, L H Tang, I M Modlin. 1. Section of Digestive Disease, Department of Internal Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029.
Abstract
OBJECTIVE: To investigate the relationship between Helicobacter pylori (Hp) infection and pathophysiology of abnormal gastric acid secretion and mucosal proliferation by studying the effect of Hp lipopolysaccharide (LPS) on the function of enterochromaffin-like (ECL) cells in vitro. METHODS: Pure isolated ECL cell preparation with a purity of +/- 95% was developed by proteinase digestion, elutriation and density gradient centrifugation with viability of > 95% as determined by trypan blue exclusion. After a short duration of culture basal and stimulated histamine secretion and DNA synthesis of ECL cells were measured by enzyme immunoassay and bromodeoxyuridine (BrdU) uptake, respectively. RESULTS: Hp LPS stimulated basal and gastrin-stimulated histamine secretion (EC(50)4 x 10(-11) mol/L and EC(50) 10(-10) mol/L respectively). These effects were completely inhibited by somatostatin (10(-10) mol/L) but not by gastrin receptor antagonist L(365 260). Hp LPS did not stimulate basal DNA synthesis but significantly increased gastrin stimulated BrdU uptake with EC(50) of 10(-10) mol/L. Escherichia coil LPS had no significant effect on both histamine secretion and DNA synthesis. CONCLUSION: Hp stimulates both ECL cell proliferation and secretion in vitro. An interaction between Hp LPS and ECL cells may contribute to the reported abnormalities in acid secretion and gastric pathophysiology noted in Hp infection.
OBJECTIVE: To investigate the relationship between Helicobacter pylori (Hp) infection and pathophysiology of abnormal gastric acid secretion and mucosal proliferation by studying the effect of Hp lipopolysaccharide (LPS) on the function of enterochromaffin-like (ECL) cells in vitro. METHODS: Pure isolated ECL cell preparation with a purity of +/- 95% was developed by proteinase digestion, elutriation and density gradient centrifugation with viability of > 95% as determined by trypan blue exclusion. After a short duration of culture basal and stimulated histamine secretion and DNA synthesis of ECL cells were measured by enzyme immunoassay and bromodeoxyuridine (BrdU) uptake, respectively. RESULTS:HpLPS stimulated basal and gastrin-stimulated histamine secretion (EC(50)4 x 10(-11) mol/L and EC(50) 10(-10) mol/L respectively). These effects were completely inhibited by somatostatin (10(-10) mol/L) but not by gastrin receptor antagonist L(365 260). HpLPS did not stimulate basal DNA synthesis but significantly increased gastrin stimulated BrdU uptake with EC(50) of 10(-10) mol/L. Escherichia coil LPS had no significant effect on both histamine secretion and DNA synthesis. CONCLUSION:Hp stimulates both ECL cell proliferation and secretion in vitro. An interaction between HpLPS and ECL cells may contribute to the reported abnormalities in acid secretion and gastric pathophysiology noted in Hp infection.