 Pepsin, a potent proteolytic enzyme. It is converted from pepsinogen produced by the chief cells by HCl at a pH lower than 5. Pepsin hydrolyzes proteins into small peptides by splitting interior peptide bonds. Peptides are further digested into amino acids by enzymes in the small intestine.
 Mucus, an acid-protective coating for the stomach secreted by several types of mucus-producing cells. The mucus and bicarbonates trapped within the mucous layer maintain a neutral pH and contribute to the so-called physiologic gastric mucosa barrier. In addition, mucus serves as a physical barrier between the cells of the gastric mucosa and the ingested material in the lumen of the stomach.
 Intrinsic factor, a glycoprotein secreted by parietal cells that binds to vitamin B12. It is essential for its absorption, which occurs in the distal part of the ileum. Lack of intrinsic factor leads to pernicious anemia and vitamin B-12 defciency (see Folder 17.1).
In addition, gastrin and other hormones and hormone-like secretions are produced by enteroendocrine cells in the fundic glands and secreted into the lamina propria, where they enter the circulation or act locally on other gastric epithelial cells.
Fundic glands are composed of four functionally different cell types.
The cells that constitute the fundic glands are of four functional types. Each has a distinctive appearance. In addition, undifferentiated cells that give rise to these cells are also present. These are the various cells that constitute the gland:  Mucous neck cells  Chief cells  Parietal cells, also called oxyntic cells  Enteroendocrine cells  Undifferentiated adult stem cells  FOLDER 17.1 Clinical Correlation: Pernicious Anemia and Peptic Ulcer Disease
Achlorhydria is a chronic autoimmune disease character-Recently, new proton pump inhibitors (e.g., omeprazole ized by the destruction of the gastric mucosa. Conse-and lansoprazole) have been designed that inhibit the quently, in the absence of parietal cells, the intrinsic factor H/K-ATPase. They suppress acid production in the pariis not secreted, thereby leading to pernicious anemia. etal cells and do not affect intrinsic factor secretion. Lack of intrinsic factor is the most common cause of vita-Although it was generally thought that the parietal cells min B12 deficiency. However, other factors such as gram-are the direct target of the H2 receptor–antagonist drugs, negative anaerobic bacterial overgrowth in the small recent evidence from a combination of in situ hybridization intestine are associated with B12 deficiency. These bacte-histochemistry and antibody staining has unexpectedly reria bind to the vitamin B12–intrinsic factor complex, pre-vealed that the immunoglobulin A (IgA)–secreting plasma venting its absorption. Parasitic tapeworm infections also cells and some of the macrophages in the lamina propria produce clinical symptoms of pernicious anemia. Because display a positive reaction for gastrin receptor mRNA, not the liver has extensive reserve stores of vitamin B12, the the parietal cells. These findings indicate that the agents disease is often not recognized until long after significant used to treat peptic ulcers may act directly on plasma cells changes in the gastric mucosa have taken place. or macrophages and that these cells then transmit their ef-