It has been established that the gut microbiota greatly influences human health by assisting in digestion of food, making certain vitamins, and aiding in the activation of the immune system. However, it is also essential to maintain a balanced community of microorganisms. As mentioned above many factors including antibiotics, stress, and certain diets all contribute to an imbalance in the gut microbiota termed dysbiosis (Hawrelak et al.,2004). Many illnesses such as Crohn’s Disease and antibiotic-associated colitis is linked to dysbiosis. Crohn’s disease (CD) is the chronic inflammation of any portion of the gastrointestinal tract. Imbalance of the gut microbiota composition is considered one of the factors that contribute to the cause of
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hypothesized that the imbalance of commensal gut flora results in inflammatory bowel diseases such as CD and ulcerative colitis (UC). To test this hypothesis, biopsies of patients with CD and UC were obtained and compared to healthy individuals. Results indicated that individuals with CD had increased levels of the Proteobacteria and Bacteriodetes phyla but decreased levels in Firmicutes in comparison to the healthy individuals. Table 1 illustrates the precise numbers of colonies. Patients suffering from CD have shown using fluorescent in situ hybridization (FISH) that commensal microflora closely contact the mucus layer that acts as one of the first lines of defense against pathogen invasion in the intestine and some are actually penetrating it (Haag et al. 2015). Petersson et al. showed that the thin colonic mucus layer of germ-free mice is restorable by introducing the lumen of the intestine to lipopolysaccharide (LPS) and peptidoglycan (PGN) of commensal microbiota (Figure 1). Dysbiosis of the gut microbiota also weakens the barrier controlled by tight junctions, desmosomes, and adherence jynctions in-between epithelial cells. Weakening the barrier increases the permeability of the epithelium which in turn allows for the passage of more
hypothesized that the imbalance of commensal gut flora results in inflammatory bowel diseases such as CD and ulcerative colitis (UC). To test this hypothesis, biopsies of patients with CD and UC were obtained and compared to healthy individuals. Results indicated that individuals with CD had increased levels of the Proteobacteria and Bacteriodetes phyla but decreased levels in Firmicutes in comparison to the healthy individuals. Table 1 illustrates the precise numbers of colonies. Patients suffering from CD have shown using fluorescent in situ hybridization (FISH) that commensal microflora closely contact the mucus layer that acts as one of the first lines of defense against pathogen invasion in the intestine and some are actually penetrating it (Haag et al. 2015). Petersson et al. showed that the thin colonic mucus layer of germ-free mice is restorable by introducing the lumen of the intestine to lipopolysaccharide (LPS) and peptidoglycan (PGN) of commensal microbiota (Figure 1). Dysbiosis of the gut microbiota also weakens the barrier controlled by tight junctions, desmosomes, and adherence jynctions in-between epithelial cells. Weakening the barrier increases the permeability of the epithelium which in turn allows for the passage of more