Helicobacter pylori, a gram-negative microaerophilic pathogen, causes several upper gastrointestinal diseases, such as chronic gastritis, peptic ulcer disease, and gastric cancer. For the diseases listed above, H. pylori has different pathogenic mechanisms, including colonization and virulence factor expression. It is essential to make accurate diagnoses and provide patients with effective treatment to achieve positive clinical outcomes. Detection of H. pylori can be accomplished invasively and noninvasively, with both having advantages and limitations. To enhance therapeutic outcomes, novel therapeutic regimens, as well as adjunctive therapies with probiotics and traditional Chinese medicine, have been attempted along with traditional empiric treatments, such as triple and bismuth quadruple therapies. An H. pylori infection, however, is difficult to eradicate during treatment owing to bacterial resistance, and there is no commonly available preventive vaccine. The purpose of this review is to provide an overview of our understanding of H. pylori infections and to highlight current treatment and diagnostic options.

Helicobacter pylori is a gram-negative microaerophilic microorganism intricately associated with chronic gastrointestinal disorders and gastric cancer. H. pylori can cause various upper digestive tract diseases, including chronic gastritis, peptic ulcer, gastroesophageal reflux disease, and gastric cancer. The bacterium exhibits a variety of pathogenic mechanisms, including colonization, the expression of virulence factors, and the development of drug resistance. This article presents a comprehensive review of H. pylori pathogenesis, emphasizing recent research advancements concerning the cytotoxin-associated gene A, vacuolating cytotoxin, outer membrane proteins, and other virulence factors. Additionally, it examines the molecular mechanisms underlying drug resistance and evaluates the efficacy of conventional therapeutic approaches. Recently, researchers have attempted novel therapeutic regimens, including probiotics and Chinese medicine-assisted therapies, to enhance therapeutic effects. This article aimed to offer an overview of the academic community’s comprehension of H. pylori infection and to highlight the current treatment options.

Background. Administration of nonsteroidal anti‐inflammatory drugs (NSAIDs) often causes small intestinal ulcers in patients, but few effective drugs are currently available to manage such serious adverse events of NSAIDs. Li‐Zhong decoction (LZD), a well‐known traditional Chinese medicine (TCM) formula, is commonly prescribed for treatment of gastrointestinal diseases. The present study aimed to investigate the anti‐ulcerogenic activity of LZD on indomethacin‐ (IND‐) induced duodenal ulcer in rats. Mechanistic studies of action of LZD were focused on involvement of TLR‐2/MyD88 signaling pathway. Methods. Fifty male Sprague‐Dawley (SD) rats were randomly and evenly divided into five groups: normal control, ulcer control (IND, 25 mg/kg), IND + esomeprazole (ESO, 4.17 mg/kg), and IND + low and high doses of LZD (3.75 and 7.50 g/kg). Macroscopic and histopathological examinations were performed for evaluation of ulcer index (UI), curative index (CI), and microscopic score (MS). Levels of duodenal inflammatory biomarkers and cytoprotective mediators including interleukin‐4 (IL‐4), IL‐10, tumor necrosis factor‐α (TNF‐α), and prostaglandin E₂ (PGE₂) were measured by ELISA. Expression levels of TLR‐2 and MyD88 mRNA were assessed by qRT‐PCR. The expression and distribution of TLR‐2 and MyD88 proteins were analyzed by western blot and immunohistochemistry, respectively. Results. Gross and microscopic examinations of the IND‐treated rats revealed severe duodenal hemorrhagic necrosis, inflammatory infiltration, villus destruction, and crypt abscess, while LZD‐treated rats manifested these pathological events to a markedly lesser degree. LZD significantly decreased UI and MS, increased CI, preserved the integrity of the villus and crypt, and normalized the tissue architecture of the duodenum of rats. The elevated TNF‐α levels in the IND‐treated rats were markedly diminished in the LZD‐treated rats, while lower levels of IL‐4, IL‐10, and PGE₂ observed in IND‐treated rats were significantly increased in LZD‐treated rats. Interestingly, improvement of immune function in duodenal mucosa by reduction of mRNA and protein expression levels of TLR‐2 and MyD88 was also observed in rats treated with LZD. Consistently, immunohistochemical analyses revealed a lower co‐localization of TLR‐2 and MyD88 proteins in the duodenal mucosa of LZD‐treated rats as compared to the IND‐induced rats. Conclusions. Our data demonstrate that LZD protects the duodenal mucosa from IND‐caused lesions, which is at least partially attributable to the interaction of its potential cytoprotective and anti‐inflammatory mechanisms together with enhancement of the mucosal immunity through TLR‐2/MyD88 signaling pathway.