-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
pylori) is a spiral-shaped, microaerobic, gram-negative bacterium
that parasitizes the human gastric mucosa.
Its discoverer won the 2005 Nobel Prize
in Medicine and Physiology.
So far, a large number of studies have confirmed that Helicobacter pylori infection is closely related to the onset of gastrointestinal diseases such as gastritis, peptic ulcer, gastric adenocarcinoma, gastric mucosa-related
lymphoid tissue lymphoma.
The pathogenesis of H.
pylori infection is complex
.
The chemotaxis adhesion ability, virulence characteristics, host susceptibility and external environmental factors of the strain are the main factors affecting Hp infection, among which chemotaxis adhesion and colonization are important steps of Hp infection, and Hp colonized the gastric mucosa interacts with host cells to produce a certain inflammatory response by releasing virulence factors, which eventually leads to clinical results
such as chronic inflammation, ulcers, and cancer.
The flagella of the bacterium provide the power to cross the mucus layer
.
adhesion, it firmly adheres to epithelial cells and avoids being emptied
by the stomach along with food.
03
Secretion of vacuole toxins (VacA gene) and cytotoxin-associated proteins (CagA genes) are the main toxic substances
.
The production of urease decomposes urea to produce ammonia, in addition to the protective effect against Helicobacter pylori, can also directly and indirectly cause gastric mucosal barrier damage
.
Secrete peroxide dismutase (SOD) and catalase to protect it from neutrophil killing, secrete mucinase, lipase, phospholipase A, lipopolysaccharide and other degradation fluids, and destroy the integrity
of gastric epithelial cells.
Helicobacter pylori produces antibodies through antigen mimicking, resulting in immune damage
to gastric mucosal cells.
It should be noted that some pathogenic agents function at multiple stages, such as adhesion plays an important role
in environmental modification and colonization adhesion and even immune damage.
Flagella not only play a role in colonization, but also have a certain influence
on immune damage and regulation.
References:
1.
WU Shenghai, WANG Xianjun.
Research progress on pathogenic mechanism of Helicobacter pylori[J] .
International Journal of Epidemiology and Epidemiology,2011,38(02 ): 134-137.
]
2.
LUO Wei, SUN Ying, ZHANG Xiaofang, et al.
New progress in the study of pathogenic factors of Helicobacter pylori[J] .
International Journal of Immunology,2019,42(4): 402-406.
3.
WANG Gaihao, DAI Fei, ZHAO Hongzhen, et al.
Research progress in molecular immunology of pathogenesis mechanism of Helicobacter pylori[J] .
Chinese Medical Journal, 2016, 96(44): 3609-3613.
4.
ZHU Yueyong,ZHUANG Zehao,DONG Jing.
Gastroenterologist's Handbook of Ward Rounds (2nd Edition)[M].
Beijing:Chemical Industry Press,2017.
