Immune Response in H. pylori-Associated Gastritis and Gastric Cancer

Abstract

Helicobacter pylori (H. pylori) is the dominant member of the gastric microbiota and has infected more than half of the human population, of whom 5–15% develop gastric diseases ranging from gastritis and metaplasia to gastric cancer. These diseases always follow inflammation induced by cell surface and intracellular receptors and subsequent signaling, such as the NF-κB pathway and inflammasomes. Some types of immune cells are recruited to enforce an antibacterial response, which could be impeded by H. pylori virulence factors with or without a specific immune cell. Following decreased inflammation, neoplasm may appear with a little immune surveillance and may inhibit antitumor immunity. Therefore, the balance between H. pylori-associated inflammation and anti-inflammation is crucial for human health and remains to be determined. Here, we discuss multiple inflammation and immunoregulatory cells in gastritis and summarize the main immune evasion strategies employed by gastric cancer.

Helicobacter pylori Subdues Cytokine Signaling to Alter Mucosal Inflammation via Hypermethylation of Suppressor of Cytokine Signaling 1 Gene During Gastric Carcinogenesis

“…The immune response to the H. pylori infection in the gastric mucosa is typically associated with the release of inflammatory and anti-inflammatory cytokines from different types of immune cells like Th1, Th2, Th17, macrophages, monocytes, mast cells and neutrophils. Many of these cytokines such as IL1, IL2, IL6, IL10, IL17, IL23, TNF-α, TGF-β, IFN-γ, CXCL12, and CXCL4 are secreted both at the site of infection and in the general blood circulation ( 16 ). Specific membrane receptors are expressed by gastric epithelial cells that help to transmit the signal carried by different cytokines to the cell interior ( 17 ).…”

The clinical efficacy and safety of atropine combined with omeprazole in the treatment of patients with acute gastritis: a systematic review and meta-analysis

“…The integrity of the gastrointestinal mucosa is maintained by mucus, gastric epithelium, bicarbonate, and gastric mucosal blood flow. When the integrity of the mucosa is destroyed, aggressive factors such as pepsin, bile reflux, cigarettes, alcohol, nonsteroidal anti-inflammatory drugs, and Helicobacter pylori (2) can cause varying degrees of gastrointestinal damage (3). The main clinical manifestations are gastrointestinal symptoms such as abdominal pain, bloating, nausea, and vomiting.…”

Gastric histopathological features after the administration of omeprazole, amoxicillin, and clarithromycin in gastritis Helicobacter pylori rat model

“…The disruption of the balance of these two groups of factors, predominating the aggressive factors, promotes gastroduodenal pathologic lesions. Clinically, the lesions vary depending on the severity of gastroduodenal damage [ 2 ]. In day-to-day clinical practice, gastritis, an inflammation of the gastric mucosa, and gastroduodenal infections are assessed to be over 80%, brought about by H. pylori [ 3 ].…”