Ma è davvero tutta colpa dell'#Helicobacter #Pylori?Ne parliamo insieme al collega Gabriele Prinzi.

What is Helicobacter pylori? Helicobacter pylori is a Gram-negative, helix-shaped bacterium capable of colonizing the stomach and disrupting the organ's homeostasis. The mechanism by which the bacterium resists stomach acidity is explained by the enzymatic action of urease, which hydrolyzes the urea present in the stomach, producing ammonia and CO₂ that increase gastric pH, creating a favorable environment for the bacterium, which is why it is not killed by acidic pH. The activity of bacterial urease is increased by a heat shock protein (HspB), co-expressed with urease on the surface of the bacterium. It is one of the dominant proteins recognized by most people infected with Helicobacter pylori. The CagA toxin, encoded by the cagA gene, is associated with a high risk of severe gastritis, peptic ulcer disease, and gastric adenocarcinoma, as well as gastric lymphoma and gastric mucosa-associated lymphoma (MALT). It is injected into gastric epithelial cells by the type IV secretion system, deregulating intracellular signaling pathways. After secretion, the toxin undergoes tyrosine phosphorylation by a kinase belonging to the Src family, regulating cell growth and motility. Furthermore, the study reported below has shown that it interacts with SHP-2 tyrosine phosphatase, alterations of which predispose to genetic and epigenetic changes involved in gastric carcinogenesis. Finally, other components of the bacterium include lytic enzymes (lipases, phospholipases, and proteases) that modify the gastric surface mucus. Consequences of Helicobacter Pylori Attack Helicobacter pylori penetrates the mucous layer of the stomach and adheres to the surface of gastric mucosal cells. It uses urease to produce ammonia from urea, neutralizing gastric acidity. This produces an infectious focus, leading to mucosal destruction (via the VacA toxin) and inflammation (via CagA). The bacterial attack, therefore, initially leads to the development of chronic gastritis, then to ulcerative lesions, as it causes mucosal damage and disrupts acid secretion. Furthermore, an imbalance occurs between aggressive factors (bacteria) and protective factors (gastric acidity), and the damage is amplified through the release of inflammatory mediators. Following ulceration, the damage can extend to gastric cancer; In fact, chronic active gastritis causes gastric atrophy, followed by gastric cells transforming into cells of the duodenal glands, leading to intestinal metaplasia and, ultimately, cancer. Helicobacter Pylori: Friend or Foe? Stomach cancer occurs when the CagA toxin, which over time causes chronic inflammation of the gastric wall cells, can eventually promote the development of genetic mutations. Can it be a protective factor? Helicobacter Pylori has always been viewed as a harmful bacterium, although it has been shown that some strains of this bacterium can play a protective role by preventing the formation of tumors in the cardia (the cardia is the sphincter that allows communication between the esophagus and the stomach). This is because it reduces the acidity of gastric juices, which could irritate the esophageal walls, reducing the harmful stimuli that lead to tumor development. Furthermore, the same phenomenon reduces the risk of esophageal adenocarcinoma in people who suffer from it chronically. Some studies also confirm the potential beneficial effect of Helicobacter pylori on the immune system: two American infectious disease specialists, Chen and Blaser, discuss the relationship between allergies and intestinal inflammation. Read the full article on my website: https://www.francescogarritano.it/nut... 🔻🔻🔻 VISIT MY CHANNELS 🔻🔻🔻 ✅ Follow my Facebook page   / francesco.garritano.biologo.nutrizionista   ✅ Follow my Instagram account   / dott.francescogarritano   ✅ Find me on LinkedIn   / francesco-garritano   ✅ Join my Telegram channel https://t.me/dottfrancescogarritano Join my digital communities on Facebook, you'll find lots of interesting content: 🔸 Hashimoto's Thyroiditis, Hypothyroidism, and Nutrition   / 1899415573608507   🔹 Fibromyalgia and Nutrition   / 344658302676528   🔺 Endometriosis and Nutrition   / 2492897660767452   ▶️ Small Intestine Bacterial Overgrowth (SIBO)   / 347354065880915   If you need advice or more information, contact me: ✉️ [email protected] 📞 392 009 2540