Human Gastric Biomarkers
Amidated gastrin-17 is a biologically and physiologically important molecule among the family of the gastrin peptides. Amidated gastrin-17 is the most powerful gastrin peptide in the feedback control mechanism of the acid secretion and output from the parietal cells in the gastric corpus. This peptideis solely synthetized and secreted into the circulation by the so called G cells (“gastrin cells”) in the gastric antrum. A positive immunohistochemical reaction for gastrin-17 is a sign of a highly differentiated gastrin-secreting cell and normal antral mucosa. In atrophic gastritis, the normal antral (pyloric) glands and gastrin-17 synthetizing cells disappear. Metaplastic pyloric glands (pseudopyloric metaplasia) do not contain immunopositive gastrin-17 cells.
Pepsinogen I is a group of precursor molecules for pepsin. These proteins are solely synthetized and secreted into gastric lumen by chief (pepsin) cells and mucous neck cells in the gastric corpus (oxyntic mucosa). In atrophic corpus gastritis these cells disappear resulting in a decrease of the serum level of pepsinogen I and in a reduction of the number of pepsinogen I positive cells in gastric biopsies. The presence of positive immunostaining for pepsinogen I is a highly reliable sign for the acid-secreting oxyntic glands. In gastric heterotopia of the duodenal bulb, but not in gastric metaplasia, the oxyntic-type glands give a positive immunohistochemical reaction for pepsinogen I.
Pepsinogen II is a group of precursor molecules for pepsin. These proteins are secreted into the gastric lumen by the pyloric glands of the gastric antrum and also by the chief and neck cells of the gastric corpus (oxyntic mucosa). Negative immunohistochemical reaction for pepsinogen I (right) but positive reaction for pepsinogen II (left) is a typical sign of the antral mucosa and, in the presence of atrophic gastritis, this staining pattern indicates that the positive glands and cells are metaplastic and “pyloric” in differentiation (so called pseudopyloric metaplasia).