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H. pylori is able to adhere to the surface of the phagocytes and impede their action. This is responded to by the phagocyte in the generation and release of oxygen metabolites into the surrounding space. H. pylori can survive this response by the activity of catalase at its attachment to the phagocytic cell surface. Catalase decomposes hydrogen ...
Atrophic gastritis under low power. H&E stain. Autoimmune metaplastic atrophic gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor. [6] Achlorhydria induces G cell (gastrin-producing) hyperplasia, which leads to hypergastrinemia.
This causes an immune response, resulting in common symptoms as phagocytes break down the bacteria within the host. Some bacteria, such as H. pylori, can secrete toxins into the surrounding tissues, resulting in cell death or inhibition of normal tissue function. Viruses, however, use a completely different mechanism to cause disease.
Helicobacter heilmannii s.s. (H. heilmannii s.s.) is a species within the Helicobacter genus of Gram negative bacteria. [1] Helicobacter pylori (H. pylori) is by far the best known Helicobacter species primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the non-lymphoma type, and ...
While a host's homologous recombination can act as a defense mechanisms for fixing DNA double stranded breaks (DSBs), it can also create changes in antigenic DNA that can create new, unrecognizable proteins that allow the antigen to escape recognition by the host's immune response. Through the recombination of H. pylori's outer membrane ...
Gastritis caused by H. pylori infection is ... The immune system makes proteins and ... Intestinal metaplasia typically begins in response to chronic mucosal injury ...
The inflammatory response induced by TLR5 during H. pylori is also considered to be possibly flagellin independent. This suggests that an unknown H. pylori factor is responsible for this response [12] In addition to inflammation induction, TLR5 is also shown to enhance gastric cancer cell proliferation through an ERK-dependent pathway. [29]
The Le(b) and H antigens are receptors for the bacteria Helicobacter pylori, a gram-negative bacterium that can cause gastritis and has been implicated in peptic ulcer disease, gastric adenocarcinoma, mucosa-associated lymphoma (or mucosal associated lymphatic tissue lymphoma – MALToma) and idiopathic thrombocytopenic purpura (ITP). [7] [8] [9]
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