Association ofHelicobacter pyloriand iNOS Production by Macrophages and Lymphocytes in the Gastric Mucosa in Chronic Gastritis

Abstract

Helicobacter pylori is one of the most common causes of chronic gastritis. With the development of the disease cellular inflammatory infiltrates composed of lymphocytes, plasma cells, and macrophages are formed in epithelium and lamina propria of the stomach. These cells are capable of secreting a number of active substances, including inducible nitric oxide synthase (iNOS). We examined the relationship between H. pylori and secretion of iNOS by cells of inflammatory infiltrates in chronic gastritis by light microscopy and immunohistochemistry. The data obtained indicate that stimulation of H. pylori immune system cells of the host organism during development of chronic gastritis causes increase in number of macrophages and lymphocytes in the inflammatory infiltrate of the gastric mucosa. This is accompanied with increased expression of inducible NO-synthase with excess free radicals in the tissues, which leads to secondary alterations and exacerbates the inflammation with impaired regeneration processes.

Carbon monoxide released from its pharmacological donor, tricarbonyldichlororuthenium (II) dimer, accelerates the healing of pre‐existing gastric ulcers

“…Granulocyte and macrophage infiltration is increased at the ulcer margin, and it has been suggested that this could be the major source of increased COX‐2 expression that is positively regulated by IL‐1β and TNF‐α (Takahashi et al ., ; Shigeta et al ., ; Jackson et al ., ). Moreover, the increased infiltration of macrophages followed by an up‐regulated NOS expression has been observed during the development of chronic gastritis (Cherdantseva et al ., ). We observed that CORM‐2 decreased mRNA and protein expression of pro‐inflammatory factors such as iNOS, as well as COX‐2.…”

Cooperation of Gastric Mononuclear Phagocytes with Helicobacter pylori during Colonization

“…While effector immune mechanisms of elimination have not been dissected in depth, the type of immune response elicited may depend on the location and kind of cell that first comes in contact with H. pylori . Colonization of the gastric mucosa by H. pylori induces mixed effector and regulatory immune responses (11). However, its chronic persistence in the host suggests that the regulatory immune responses might predominate over effector mechanisms (12–20).…”

Impact of nitric oxide's bidirectional role on glaucoma: focus onHelicobacter pylori–related nitrosative stress

“…Upon Hp gastric mucosa colonization, an immune response is induced. Mucosal migration of macrophages and lymphocytes producing iNOS also takes place . Once lymphocytes, plasma cells, and macrophages are chemotactically triggered, iNOS is generated, as seen by elevated concentrations of NO metabolites in Hp ‐infected patients .…”

“…Mucosal migration of macrophages and lymphocytes producing iNOS also takes place . Once lymphocytes, plasma cells, and macrophages are chemotactically triggered, iNOS is generated, as seen by elevated concentrations of NO metabolites in Hp ‐infected patients . Chronic antigenic stimulation, such as by superficial bacterial LPS upon exposure to inflammatory cells, regulates iNOS expression in order to generate NO and RNS.…”