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Unique to the human body due to its acid-secreting ability, the parietal cell has always been a subject of interest for scientific research. Harbored in the gastric glands of the fundus and body, parietal cells are considered to be dynamic, as they undergo morphological transition during the resting and secretory states.[1][2] Parietal cells play a pivotal role in gastric homeostasis, as well as in the absorption of vitamin B12 (cobalamin) due to the release of intrinsic factor (IF).[3] Paracrine, endocrine, and neural pathways are involved in the rigorous control of acid secretion by parietal cells.[4] Therefore, they play an important role in gastric pathologies and are considered to be crucial in the pathophysiology of acid reflux disease, different causes of gastritis, pernicious anemia, Helicobacter pylori infection, among others.[5] It is imperative to understand their physiology, structure, and clinical relevance to grasp the importance of the said cells in the gastric environment.

There are a variety of pathologies that affect parietal cell gastric acid secretion, as well as intrinsic factor secretion. The most common cause of gastric pathology worldwide is Helicobacter pylori infection.[5] This pathogen has correlations with gastritis, atrophic gastritis, peptic ulcer, and gastric cancer.[5] H. pylori have many virulence factors that promote cellular adhesion (BabA/B, sabA, OipA), evasion of the immune response (LPS), and cell damage mediated through disruption of tight junctions (Ure A/B).[5] Regarding progression to gastric cancer, the cytotoxin-associated gene A (CagA) is considered to be pro-inflammatory and correlates with the development of gastric neoplasia, since it promotes p53 degradation, downregulating the apoptosis-stimulating protein of p53 tumor-suppressor pathway.[5][17] H. pylori correlate with hypochlorhydria mediated by interruption of interactions between parietal cells, G cells, ECL cells, and D cells.[8] Furthermore, infection with this pathogen, through endoplasmic reticulum stress, induces overexpression of cation transport regulator 1 (CHAC1), an enzyme involved in the degradation of glutathione into 5-oxoproline and cysteinyl-glycine, which eventually results in intracellular depletion of glutathione, culminating in unbalanced cellular redox levels.[18] Autoimmune gastritis is associated with the loss of parietal cells in the body and fundus, and it accounts for 10% of chronic gastritis cases.[3] It is associated with autoantibodies against parietal cells and intrinsic factors. IgG or IgA targets H/K ATPase, which leads to atrophic gastritis limited to the body and fundus.[7][5] Autoimmune gastritis is also associated with iron-deficient anemia, a condition known as “achylia gastrica.”[19] This is considered to be caused by the destruction of ascorbic acid in the gastric lumen due to a higher pH.[19] Also, this results from the inability to free iron from proteins without the action of gastric acid.[19] Pernicious anemia is one of the late manifestations of autoimmune gastritis, resulting from the deficiency of vitamin B12 due to autoantibodies against parietal cells and intrinsic factor.[19][20] This deficiency leads to cobalamin malabsorption in the terminal ileum and eventual, megaloblastic anemia.[21]

Autoimmune gastritis is associated with the loss of parietal cells in the body and fundus, and it accounts for 10% of chronic gastritis cases.[3] It is associated with autoantibodies against parietal cells and intrinsic factors. IgG or IgA targets H/K ATPase, which leads to atrophic gastritis limited to the body and fundus.[7][5] Autoimmune gastritis is also associated with iron-deficient anemia, a condition known as “achylia gastrica.”[19] This is considered to be caused by the destruction of ascorbic acid in the gastric lumen due to a higher pH.[19] Also, this results from the inability to free iron from proteins without the action of gastric acid.[19] Pernicious anemia is one of the late manifestations of autoimmune gastritis, resulting from the deficiency of vitamin B12 due to autoantibodies against parietal cells and intrinsic factor.[19][20] This deficiency leads to cobalamin malabsorption in the terminal ileum and eventual, megaloblastic anemia.[21] Prostaglandins are responsible for protecting the gastric mucosa from injuries caused by hydrochloric acid. NSAIDs cause gastritis by inhibiting the production of prostaglandins, which gets mediated by inhibition of cyclo-oxygenase.[5][22]