How is Helicobacter pylori adapted to life in the stomach? Describe it's coping mechanism.
H. pylorus reaches homeostasis within in the stomach in several ways. One way is that the bacterium embeds itself in the mucus of the stomach lining which is less acidic. Another way is that H. pylori has evolved in such a way that it can manipulate the levels of stomach acid. When acid levels are too low the H. pylori becomes endangered by other bacteria that may encroach on its environment so the organism stops causing inflammation and damage to the stomach lining, thus the acid levels rise. When the acid level is too high H. Pylorus creates more inflammation and damage causing the stomach to produce less acid. The last method the bacterium utilizes to survive in the stomach is that it is able to produce a toxin which inhibits the stomachs autoimmune response.
Describe how H. pylori induces gastric ulcers.
H. pylorus with the Cag A gene encode TFSS proteins that assemble into miniature hypodermic needles which injects the Cag A protein into the epithelial cells that line the human stomach. The holes or vacuoles weaken the lining of the stomach and lead to gastric ulcers. In addition, H. pylorus produces a toxin named Vac A which in addition to causing vacuoles also suppresses the production of white blood cells in the stomach diminishing the autoimmune response.
What is the evolutionary advantage for H. pylori to produce a “slow” chronic infection?
The evolutionary advantage for H. pylori producing a slow chronic infection is related to its ability to evolve into a symbiotic relationship with its host by creating a negative feedback loop involving various H. pylori cells as well as host cells. The evolution has enabled the host to minimalize damage from infection by developing ways to signal to the bacteria through immune responses and changes in the pressure and acidity of the stomach. The H. pylorus has evolved a way to signal host cells to alleviate...