Helicobacter pylori (H.pylori)

Helicobacter pylori (H.pylori) is a gram-negative microaerobic bacterium that infects nearly half of the world's population, and persistent infection with this bacterium leads to chronic gastritis. 1994, the World Health Organization has classified H.pylori as a class I carcinogen.

 

In addition, the role of H. pylori in the development of peptic ulcers, gastric cancer and, rarely, gastric MALT lymphoma has been well recognized. In addition to the direct pathogenic effects, the alteration of gastric motility, pH, and barrier function by H. pylori indirectly affects the gastric flora homeostasis. With the widespread use of high-throughput sequencing technology, more bacteria are continuously being detected, and a large number of studies have investigated the effects of H. pylori on the gastric flora. The composition of the gastric flora may be influenced by factors such as H. pylori colonization, patient's diet, drug use, age, and gastric mucosal inflammation, and H. pylori is likely to be a key node in understanding the complex interactions between the human body and the gastric flora network. Therefore, elucidation of H.pylori-induced gastric endoflora dysregulation provides a broader perspective for a deeper understanding of the relevant gastric pathological processes.

 

KMD Bioscience, as a manufacturer of in vitro diagnostic reagents, provides raw materials such as antibodies, antigens, enzymes and nanomaterials for in vitro diagnostics. KMD Bioscience has several mature technology platforms, including immunochromatography, latex turbidimetry, chemiluminescence and molecular diagnostics. Our main products are in vitro diagnostic antigens (natural antigens, genetically engineered recombinant antigens), antibodies (monoclonal antibodies, polyantibodies), fluorescent microspheres, etc., which cover a wide range of fields such as cardiovascular, renal, hormonal, diabetes, infectious diseases, autoimmune diseases and so on.

 

The inventory of reagents associated with Helicobacter pylori (H.pylori) that KMD Bioscience can offer:

 

 

CAT#

Product Name

Species

Host

Application

Size

Inquiry

PA265

Mouse Anti-H. Pylori Monoclonal Antibody (Detection)

Human

Mouse

LFIA (Lateral-Flow Immunochromatographic Assay), CLIA (Chemiluminescence Immunoassay), ELISA

1mg

Inquiry

PA266

Mouse Anti-H. Pylori Monoclonal Antibody (Capture)

Human

Mouse

LFIA (Lateral-Flow Immunochromatographic Assay), CLIA (Chemiluminescence Immunoassay), ELISA

1mg

Inquiry

 

Functional Characterization of H. pylori

 

After entering the human body, Helicobacter pylori (HP) can be customized in the gastric mucosa for a long period of time, and can produce a variety of enzymes, including urease, protease, peroxidase, and lipase, as well as a number of other pathogenic factors, which can cause inflammatory damage to the gastric mucosa and disrupt the balance between proliferation and apoptosis of gastric epithelial cells. The infection can be eliminated by standard anti-H. pylori treatment. Helicobacter pylori has been classified as a class I carcinogen by WHO (World Health Organization).

 

1、Biological characteristics of Helicobacter pylori

 

HP belongs to the family of Vibrio, is a spiral, gram-negative microorganisms. HP has little resistance to the external environment, sensitive to dryness and heat, and can be killed by a variety of commonly used disinfectants. In 4 ℃ water can survive for 1 year, in room temperature air can only survive for a few hours. HP on the growth of very demanding conditions, micro-oxygenation, need to grow in nutrient-rich medium, the optimal growth temperature of 37 ℃, pH value of 5.5 ~ 8.5 range can grow.

 

2、Pathogenicity

 

(1) The infection mainly in the gastric sinus increases the secretion of gastrin, which may damage the secretion of local growth inhibitor. The high gastric acid secretion it causes accelerates the formation of prepyloric and duodenal ulcers.

 

(2) Infections predominantly of the gastric body cause atrophic gastritis and decrease gastric acid secretion, probably due to increased local interleukin-1β production. Patients with predominantly gastric body infections are more likely to develop gastric ulcers and gastric adenocarcinoma. Some patients have mixed sinus and gastric body infections.

 

(3) Patients with Hp infection are 3-6 times more likely to develop gastric cancer. Hp infection has been associated with intestinal-type adenocarcinoma of the gastric body and gastric sinus, but not gastric cardia. Other associated tumors include lymphoma and mucosa-associated lymphoid tissue (MALT) lymphoma, and monoclonal restrictive B-cell tumors.

 

(4) HP infection may also be associated with the development of a number of extragastric diseases, such as atherosclerosis-associated disease, primary Raynaud's phenomenon, primary headache, biliary tract infections, chronic liver disease, diabetes mellitus, urticaria, and pemphigus.

 

Relationship between H. pylori and gastritis

 

Although the mechanism of H. pylori-associated gastritis is unknown, the interaction between the bacteria and gastric epithelial cells may be the determining factor. In particular, the inflammatory effect is induced by the cytotoxin associated gene A (CagA) protein.DNA damage response protein 1 (regulated in development and DNA damage responses-1, REDD1) is a conserved and ubiquitous protein that transiently induces responses in response to a variety of stimuli. involved in H. pylori infection and is an endogenous inhibitor of the mTOR signaling pathway.

 

It has been demonstrated that as an endogenous inhibitor of mammalian target of rapamycin (mTOR) signaling pathway, REDD1 regulates cell growth, mitochondrial function, oxidative stress and apoptosis. In different inflammatory diseases, REDD1 can exert opposite effects.

 

H. pylori adheres to gastric epithelial cells, and the bacterial virulence factor cagA is injected into host cells via the type IV secretion system, activating several signaling pathways, including the JAK-STAT3, PI3K-AKT, and Wnt-β-catenin signaling pathways. In gastric epithelial cells, H. pylori induced REDD1 expression-dependent activation of the MAPKp38 signaling pathway by cagA. Non-phosphorylated cagA activity has been reported to favor epithelial cell proliferation and pro-inflammatory responses.H.pylori infection leads to an increase in REDD1 in gastric epithelial cells, which is mediated by the virulence factor cagA, and plays an important role in H.pylori-induced gastritis.

 

KMD Bioscience (KMD Bioscience) has an excellent in vitro diagnostic reagent development platform, all raw materials have been repeatedly validated by multiple application platforms and a large number of clinical samples, and under strict production process control, we can continuously and stably provide high-quality raw materials for our IVD customers. Most of our antigenic raw materials are prepared by mammalian expression system, the structure and activity are closer to natural antigen. Each antigen is produced through rigorous program design, strict performance evaluation, and has excellent stability and specificity. Moreover, our antigenic materials can be used in the development of standards, calibrators, quality control products and as immunogens.