Microbiome-Model
Alexander Munoz
When the human intestinal microbiome was initially discovered, it was believed to be a solely harmful thing. For example, early scientists believed that increased populations of intestinal flora could explain gut-related pathologies. However, it was subsequently discovered that there was no correlation between quantity of intestinal microbiotal colonies (measured via colony forming units / gram of stool) and gut-related pathologies. Researchers thus concluded that intestinal bacterial species are commensal (i.e. they do not appear to harm the host). Later, it was furthemore discovered that human hosts are actually quite dependent on their intestinal microbiomes and are more mutualistic than commensal. For example, microbiotal species in the intestines produce Vitamin K (a clotting factor) and further breakdown nondigestible food, providing the host with nutrient-rich short-chain fatty acids (which interestingly also have trophic effects on the intestinal enterocytes). I chose to investigate the first of these two situations: the commensality of intestinal bacteria. Although bacteria do have trophic and metabolic effects on the host, for the purpose of this project, I will ignore those effects and focus on the pathogenecity of the bacteria. In fact, the most significant effect of bacteria on the host is not their metabolic effects nor their trophic effects - but just their existence, through witch commensal bacteria serve a purpose called competitive exclusion. There is a finite amount of surface area in the intestines, and to survive, a bacterium must attach to the mucosal wall of the intetines. Thus, there are a finite amount of bacteria that can attach to the surface area of the colon. Just by existing, commensal bacteria take up the space on the intestinal wall that would be required for the growth of pathogenic bacteria. Thus, when a normal, healthy micriobiome is presented with a pathogen, the pathogen will rarely colonize, because the space has already been taken by the host's commensal bacteria (thus the name "competitive exclusion"). Recently, observational research has shown that broad-spectrum antibiotic treated patients, hypersensitive immune system patients (i.e. inflammatory bowel diseases), and Cesarean section-birthed children all have increased risk of developing gut-bacteria related pathologies. In this project, I will investigate if these idiopathic conditions can be explained by discrepancies in commensal bacteria competitive exclusion.