Molecular mechanisms involved in anti-inflammatory effects of proton pump inhibitors

Abstract

PPI attenuate PMN-dependent gastric mucosal inflammation partly by interfering with NFkappaB activation in vascular endothelial cells and gastric epithelial cells, and partly by modulating the calcium concentration of PMN.

Evaluation of the Protective Effect of Brassica oleracea (L. var. acephala) in Rats with Surgically-Induced Gastroesophageal Reflux Disease

“…Studies have shown that proton pump inhibitors can exert anti-inflammatory and antioxidative effects unrelated to the inhibition of gastric acid production (29). Inactive forms of omeprazole in circulation can suppress important aspects of chronic inflammation, such as the adhesion of neutrophils to endothelium and the extravascular migration of neutrophils, leading to a reduction in the infiltration of inflammatory cells (30). In addition, studies in vitro and in clinical reports have shown that proton pump inhibitors prevent free radical production by neutrophils and block neutrophil degranulation (31).…”

Proton Pump Inhibitors Therapy for Eosinophilic Esophagitis

“…Similarly, PPIs inhibited the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial-dependent neutrophil adhesion in human umbilical vein endothelial cells stimulated with interleukin1b [26]. In addition, lansoprazole also has been found to inhibit the expression of ICAM-1 by human tracheal epithelial cells in culture [27] and to decrease the number of peripheral blood mononuclear cells that express ICAM-1 in human volunteers [28]. Overall, this impairment in neutrophil function has been related to the presence of vacuolar (v-type) inhibition by PPIs.…”

The effect of proton pump inhibitors on the gastric mucosal microenvironment

“…PPIs may also affect gastric mucosal inflammation, attenuate neutrophil functions and cause hypochlorhydria. [2][3][4] Neutrophils have long been viewed as short-lived effector cells of the innate immune system; they are recruited to the site of inflammation and generate reactive oxygen and nitrogen species. 5 With their destructive potential, neutrophils enter peripheral tissue and interact closely with host cells.…”

“…[9][10][11][12] PPIs affect the interaction of neutrophils with endothelial cells and attenuate neutrophil association with chemostatic cytokines of gastric mucosa. 2,4,13 However, the effect of PPIs on gastric mucosa and neutrophils has not been thoroughly clarified. 14,15 This study investigated the effect of PPIs on H. pylori, neutrophil infiltration and gastric antral mucosa inflammation.…”