Can Poor Water Treatment Result in H Pylori?
Getting settled is only the beginning, and many of the tricks that help H. pylori become established may also become necessary later in order to adapt to an ever-changing environment. For example, mucus is in constant turnover inside the stomach, and it is thought that the bacteria must repeat this colonization step, and burrow into newly formed mucus each time the mucus layer is shed from the stomach wall. The peculiar thing is that H. pylori’s need for some, though not all, of these acid-adaptive measures decreases once the infection has become established, suggesting that maintenance of H. pylori infection is more complicated than once thought. Following colonization, for example, the need for urease diminishes, even though it continues to be made by the bacterium in large quantities. Evidence that urease expression is not related to infection maintenance or the resulting diseases was obtained using urease inhibitors on infected tissues. These studies revealed that once the mucus layer is colonized, chemicals that inhibit the activity of the urease enzyme do not cure the H. pylori infection, nor do they prevent ulcer formation, suggesting that the main function of the urease enzyme is to protect the bacterium until it colonizes the stomach’s mucus layer. Whether this adaptive mechanism is turned on and off as the mucus layer is shed is not known.
Acid avoidance is only one method by which H. pylori retains its foothold in the stomach. Without some way to hold on to the tissue, the organism would be washed into the duodenum whenever the mucus layer is shed (a situation that undoubtedly occurs anyway in infected individuals, given that the duodenum is a major site of ulcer formation by H. pylori). To prevent detachment, H. pylori produce several types of adhesive proteins called adhesions. These proteins stick to specific lipids and carbohydrates that are normally present on the surface of the cells that line the stomach, preventing the organism from being dislodged by mechanical actions of the stomach (churning of food or the shedding of the mucus layer). A large number of adhesion genes have been identified, and experimental strains in which these genes have been inactivated have demonstrated that the genes are essential to the survival of the bacterium.
Adhesion proteins are expressed on the outer membrane of the bacterium, functioning as anchors that fasten the organism onto the surface of the stomach. Their interaction with the molecules on stomach cells is somewhat like Velcro in that the two molecules (one on the surface of the bacterium and one on the mucosal cell of the stomach) stick to one another tightly by physically adhering to one another. These interactions are highly specific (like a lock and key); any given adhesion expressed on the H. pylori surface has affinity for only a specific molecule on the stomach cell’s outer surface. For that reason, H. pylori cells express numerous different adhesions at the same time, meaning that each organism likely has multiple points of attachment with different types of molecules, making this a tight attachment, indeed.
However beneficial adhesions may be for H. pylori, some of these adhesions damage the lining of the stomach and lead to the pathology associated with infection during h. pylori treatment. Therefore, while the immune response to infection is an essential bodily function, it can also contribute to the pathology of infectious diseases, particularly chronic infections.