Fighting off the Cellular Parasite, H. Pylori
H. pylori as a Cellular Parasite
In addition to directly blocking the activities of the immune system in hand-to-hand combat, H. pylori has found ways to escape notice by the immune system. The immune system is slow to react to bacteria that live inside the host’s own cells, so if the invading organism can find its way into these cells, it has time to become well established before being detected and attacked. H. pylori has a couple of niches in which it escapes death by immune cells. One particularly interesting escape mechanism is its ability to survive inside immune cells themselves. Normally, when bacteria are engulfed by macrophages, they are promptly killed; however, some strains of H. pylori apparently produce a protein that inhibits the ability of the immune cell to kill them.
As a result, live bacteria are present inside the immune cell for up to 24 hours. H. pylori defends itself by causing the vacuoles in which it is engulfed by the macrophage to fuse together, generating one large vacuole inside of the macrophage that contains many bacteria. These large vacuoles are less efficient at killing bacteria than are numerous small vacuoles. In this way, the bacteria are able to delay being killed. It is unclear whether these bacteria later escape back into the tissue, but the fact that they can survive for several hours suggests that this is a potential reservoir of re-infection.
Another hiding place for H. pylori is in the epithelium. H. pylori lives within and beneath the mucus layer of the stomach, and a fraction of these organisms (around 10 percent) actually attach to the epithelial cells. This close association often leads to the bacteria being taken into and between epithelial cells. This is beneficial for the bacterium in several respects. Because the immune system is extremely well trained to avoid killing host cells, H. pylori can avoid attack by hiding inside them. In addition, using an antibiotic as an h pylori treatment as well as other harmful substances that might be present in the stomach are not as effective at reaching the bacteria when the organisms are enclosed within the epithelial cells. Furthermore, internalized bacteria avoid being washed away when the stomach empties its contents into the duodenum. In spite of the advantages of life inside the epithelium, however, the majority (90 percent or more) of H. pylori organisms in an infected animal or human appear to be free-living in the stomach, rather than epithelial cell parasites. H. pylori expresses them to trick the immune cells into thinking that the bacteria cells belong to the host. Because the immune system is very careful about turning its weapons upon itself, it is prevented from initiating attacks against the disguised bacteria.
This camouflaging process is a controversial topic, however, as immune reactions do occur as a result of other activities that the bacteria perform, and because other notions about the function of this protein have been suggested. Since the receptor for Lewis antigens is also expressed on the surface of the stomach’s epithelial cells, it has been suggested that the real function of this protein is to serve as an anchoring point for the bacterium. Only a minority of the germs (around 10 percent) actually attach to the epithelium, while the remaining 90 percent are distributed throughout the mucus layer. Thus, it has been argued by some scientists that the Lewis Blood Group proteins are more useful in allowing the bacteria to avoid attack by the immune system than in helping them adhere to the epithelium. Additional work on this subject will undoubtedly reveal more about the function of these proteins in the life cycle of the organism.
