(1) Background: Gastric cancer, the fourth most common cause of death from tumors in the world, is closely associated with Helicobacter pylori. Timely diagnosis, therefore, is essential to achieve a higher survival rate. In Chile, deaths from gastric cancer are high, mainly due to late diagnosis. Progranulin has reflected the evolution of some cancers, but has been poorly studied in gastric lesions. Aiming to understand the role of progranulin in H. pylori infection and its evolution in development of gastric lesions, we evaluated the genic expression of progranulin in gastric tissue from infected and non-infected patients, comparing it according to the epithelial status and virulence of H. pylori strains. (2) Methods: The genic expression of progranulin by q-PCR was quantified in gastric biopsies from Chilean dyspeptic patients (n = 75) and individuals who were uninfected (n = 75) by H. pylori, after receiving prior informed consent. Bacteria were grown on a medium Columbia agar with equine-blood 7%, antibiotics (Dent 2%, OxoidTM), in a microaerophilic environment, and genetically characterized for the ureC, vacA, cagA, and iceA genes by PCR. The status of the tissue was determined by endoscopic observation. (3) Results: Minor progranulin expression was detected in atrophic tissue, with a sharp drop in the tissue colonized by H. pylori that carried greater virulence, VacAs1m1+CagA+IceA1+. (4) Conclusions: Progranulin shows a differential behavior according to the lesions and virulence of H. pylori, affecting the response of progranulin against gastric inflammation.
Keywords: Helicobacter pylori; gastric lesions; progranulin; virulence.