Презентация на тему 3.2 Хеликобактериоз

отличающаяся преимущественной локализацией возбудителя на слизистой ЖКТ и 12-перстной

кишки.

по медицине

pylorus - привратник желудка, перекрывающий проход
из желудка в

двенадцатиперстную кишку).

для человека :

Helicobacter heilmannii – вызывает гастрит
Helicobacter pylori –

гастрит, язва
Helicobacter cinaedi - энтерит, септицимия
Helicobacter fennelliae - энтерит, септицимия
Helicobacter rappini - энтерит, септицимия
Helicobacter bilis – роль не ясна

окисляет и не ферментирует сахара
Окисляет органические кислоты

epithelial cells include alterations in mitochondrial membrane permeability and

apoptosis, stimulation of pro-inflammatory signalling, increased permeability of the plasma membrane and alterations in endocytic compartments. Multiple H. pylori factors, including CagA, disrupt the gastric epithelial barrier and might thereby facilitate passage of VacA through the epithelial layer148, 149. Within the lamina propria, VacA interferes with the activation and proliferation of T lymphocytes. Many of these effects of VacA are attributable to the formation of VacA membrane channels. m indicates mitochondrial transmembrane potential.

дыхательный тест

к Helicobacter Pylori иммунохроматографическим экспресс-методом
Набор реагентов «КреативМП-Н.Pylori» для выявления

Helicobacter Pylori иммунохроматографическим экспресс-методом ТУ 9398-002-83178876-2010 предназначен для качественного одноэтапного быстрого выявления всех изотипов (IgG, IgM, IgA) антител к Helicobacter Pylori в сыворотке, плазме или цельной крови человека. Набор предназначен для использования в клинической практике, а также для самостоятельного использования потребителем

Helicobacter рylori

фуразолидон.

Препараты висмута – лечение язвы и гастрита

Helicobacter рylori
нарушения энергетического гомеостаза (ожирение)
бронхиальная астма
аллергический ринит
атопический

дерматит
сахарный диабет
-системная иммуномодулирующую активность H.pylori

several mechanisms. Following adherence, signalling by the cag secretion

system (but not CagA per se) leads to activation of an unknown factor(s) X that leads to activation of nuclear factor-B (NF-B). NF-B translocates to the nucleus to activate transcription of pro-apoptotic genes. H. pylori can also induce apoptosis by stimulating expression of FAS and its ligand (FASL). The H. pylori protein urease can induce apoptosis by binding to class II major histocompatability complex (MHC) molecules. The H. pylori vacA gene product causes mitochondrial release of cytochrome c (cyt c), which leads to activation of caspase-3 and apoptosis. H. pylori also activates pathways that downregulate apoptosis. H. pylori binding to the epithelial-cell surface generates arachadonic acid, which is metabolized to prostaglandin E2 (PGE2) and prostaglandin 15-deoxy12,14-J2 (15d-PGJ2) by cyclooxygenase (COX) enzymes. These enzymes are inhibited by non-steroidal anti-inflammatory drugs (NSAIDs). 15d-PGJ2 is an endogenous ligand of peroxisome proliferator-activated receptor- (PPAR), a nuclear hormone receptor that heterodimerizes with the retinoid (RAR) family of nuclear receptors to activate transcription of target genes. These gene products inhibit NF-B activation, however, preventing apoptosis. The COX-generated metabolite PGE2 also attenuates apoptosis. So, H. pylori has the capacity to stimulate and inhibit gastric epithelial-cell apoptosis, which might influence the risk of gastric carcinogenesis.

which allows it to specifically interact with the SRC-homology

2 (SH2) domains of the protein tryosine phosphatase (PTP) SHP2. This interaction induces SHP2 to undergo a conformational change, which stimulates its phosphatase activity. Activated SHP2 can induce extracellular signal-regulated kinase (ERK) signalling through RAS-dependent and -independent mechanisms. Sustained deregulation of this pathway eventually leads to apoptosis in gastric epithelial cells. MEK, mitogen-activated protein kinase/ERK kinase.