Tight Junctions

difficile lies within the 19.6 kb pathogenicity locus (PaLoc) and codes for two major virulence factors and three accessory proteins [9]. Genes tcdA and tcdB encode Toxin A and Toxin B, respectively, the two major virulence factors which are part of the clostridial glucosylating toxin family [10]. Both catalyze the inactivation of Rho-GTPases, which are essential for the regulation of eukaryotic cell cytoskeleton [9]. The inactivation of Rho-GTPases causes cell death via cytoskeletal disorganization [9]. The accessory gene functions are as follows; tcdE as a putative holin protein; tcdD as a positive regulator and tcdC as a negative regulator, both of which are controlling Toxin A and B gene expression

What is the cause of C. diff and how does it affects the colon? In the colon, the C. diff spores are present in the active form. There are several different bacteria that typically reside in the colon and are part of the normal flora of the colon (). These bacteria prevent the activation of C. diff spores into the active bacterial form (). However, when antibiotics are administered for the treatment of an infection, they may kill some of the normal bacteria. This process disrupts the normal balance of gut bacteria and allows Clostridium difficile to become activated and infectious (). When C. diff becomes activated, it produces two different toxins, toxin A and B. These toxins may cause inflammation of the inner lining of the colon, resulting in pooling of white blood cells in the colon. If the inflammation is severe, it can result in destruction of the normal cells that line the inside of the colon. When these cells are destroyed they shed, and a large number of white blood cells may appear as small whitish membranes when visualized by colonoscopy (). These membranes are

Escherichia Coli, or E. coli, resides in the large intestine where it assists digestion and make up essential molecules like Vitamin K. For the most part, E. Coli poses no threat although there are few disease causing strains that can cause mild to severe food poisoning by finding its way into food supply (Timmons, Trzepacz, Duboinis-Gray). Enteropathogenic Escherichia coli, or EPEC, is a strain of diseasing causing E. Coli that is the leading cause of death in children with diarrhea in many parts of the world. EPEC colonizes in the intestine allowing the host to be invaded which can spread from person to person (Pearson, Wong fok Lung, Hartland, Giogha). Another strain of disease causing E. Coli also causes diarrhea in children is the DEC

difficile-associated colitis is à toxin-mediated disease and several virulence factors have been implicated in its pathogenesis; First, modification of normal gastrointestinal microbiota by administration of antibiotics.3 Second, Acquiring a toxigenic strain of Clostridium difficile, which produces toxins: C. difficile toxins A (TcdA), B (TcdB) 4 and binary toxin (CDT).5 Third, the host immune system response.

Marked alterations in cardiopulmonary function, leukocytes and thrombocytopenia lead to coagulopathies, increased vascular permeability and decreased organ blood flow and metabolism. This leads to decreased gastrointestinal motility, decreased perfusion of peripheral tissues and consequently shock (Stadler and Van,1989). Endotoxemia is one of the main causes of death in horses affected with gastrointestinal disease due to a physical obstruction causing strangulation and ischemic necrosis (Burrows,1981). Enterotoxins exert their effects on the mucosa of the intestine, causing disturbances of fluid and electrolytes. The enterotoxigenic E. coli causes hypersecretory diarrhoea. The important bacterial exotoxins are those produced by Clostridium spp. They may be ingested preformed, as in botulism, or produced in large quantities by heavy growth in the intestines, such as Clostridium defficile enterocolitis in horses.

Overall Scientific premise: Inflammatory bowel disorder (IBD) affects an estimated 1-1.3 million people in the US alone, according to the Centers for Disease Control and Prevention (CDC). Although immune intolerance in the gut is considered one of the factors driving disease progression, the origins of IBD remain unknown. Enteric infections play a major role and could potentially be an underlying cause of IBD (PMID:15256979). Staphylococcus aureus, an ESKAPE pathogen, one of the major causes of foodborne enteric infections. Nevertheless, there is a considerable knowledge gap as to how S. aureus can cause dysregulation and inflammation at enteric mucosal surfaces that could lead to IBD. Previous studies along these lines led to the

Clostridium tetani is a species of pathogenic bacteria which causes the disease tetanus in humans (World Health Organisation [WHO], 2008). Bacteria are prokaryotic microorganisms which contain various structural components. These components include a cell wall and outer membrane which is discovered by the gram stain procedure (Kratz, 2011). C. tetani are gram-positive bacteria therefore its cells have a thick wall however they do not possess an outer membrane ("Vaccines and immunisations," 2015). Other components include flagella which provide cell movement, pili which permit cell adhesion to surfaces such as host cells, and bacterial capsules also known as glycocalyx which prevents the cell from phagocytosis (Todar, 2012).

The integrity of the bowel wall in NEC is compromised, which leads to bacteria entering

Regardless of the pathogenic E. coli, some species are non-pathogenic strains which are normal and ecological essential inhabitants of the human and animal gastrointestinal tracts. Non-pathogenic and pathogenic E. coli differ with respect to the presence of genetic information that may

The infection process is very complex due to numerous virulent factors of the pathogen. In order to enter the small intestine a bacterium must first overcome the antimicrobial activity of saliva enzyme, lactoperoxidase and the low pH of digestive fluid in the (D 'Aoust, 1991). Cytotoxin present on the bacterial cell wall disturb membrane integrity of the host cells which contribute to bacterium attachment and to cell invasion (D 'Aoust, 1991). Salmonella attaches itself to the intestinal epithelial cells by fimbriae. Pathogens enter epithelial cells by membrane-bound vesicle, this process is known as bacteria-mediated endocytosis (D 'Aoust, 1991). Bacterium then divide and invade mucosa layer. Diarrheagenic enterotoxin is released in the intestinal lumen and into the lumen of epithelial cells. Effect of enterotoxin and local inflammation cause water and

This results not only in the abnormal assembly of tight junctions in areas colonized by H. pylori, but also alters the “composition and function of the apical-junctional complex” (OMIM SOURCE YEAR). Prolonged exposure to CagA results in dysplasia and prevents the epithelial barrier from functioning

Escherichia coli (E. coli) is a bacterium commonly found in the digestive system of humans and animals. Although it is mainly harmless and helps promote a healthy digestive system, some strains can be pathogenic and cause illness such as diarrhea, urinary tract infections, respiratory infections and even pneumonia. What makes E. coli pathogenic is the release of a toxin called Shiga. These are often referred to a Shiga toxin-producing E. coli (STEC). This particular strain lives harmlessly in the guts of animals, particularly cattle. However, when in contact with a human, it results in illness. Pathogenic E. coli is usually caught when humans ingest invisible amounts of feces that can be found in food or water. (CDC, 2014) Antibiotics may be prescribed depending on the illness. Their ability to effectively work depends on it’s composition and the bacteria it is expected to work on.

E. coli O157:H7 is a gram negative, rod shaped bacteria that is being found in many foodborne and waterborne illnesses. It is also called Hemorrhagic colitis, the acute disease caused by E. coli (EHEC) because it causes abdominal pain, and bloody diarrhea. It generally lives in the intestines of healthy humans and is generally harmless. It is also found in healthy cattle and can contaminate meat during slaughtering, as it produces a toxin that can cause illness. The E.coli O157:H7 is rare variety of E. coli that produces large quantities of one or more related, potent toxins that cause severe damage to the lining of the intestine. The Verotoxins that cause the disease are also called shiga toxins, because they were acquired from the Shigella strain. It is believed that the widespread use of antibiotics by American farmers has promoted the transfer of antibiotic resistance genes and pathogenicity islands that has led to the creation of new pathogenic strains such as E. coli O157:H7.

These studies indicate that both healthy and diarrheic calves harbor STEC in their intestine (Blanco et al., 1997; Roopnarine et al., 2007) and shed the bacteria in great quantities for several months (Cray and Moon, 1995; Widiasih et al., 2004). Shiga toxin-producing E. coli (STEC) are characterized by their ability to produce two types of shiga toxins virulence factors: shiga toxin 1 (encoded by the stx1 gene), shiga toxin 2(encoded by the stx2 gene). However, STEC isolates frequently have associated two virulence factors; intimin (encoded by the eaeA gene) and enterohaemolysins ( encoded by the hlyA) (Dean-Nystrom et al., 1997; Kang et al., 2004). Intimin is responsible for intimate attachment of STEC to intestinal cells, causing formation of the characteristic attaching and effacing (A/E) lesions (Bolton, 2011). Although the role of enterohemolysin in an intestinal disease is unclear, but it has been suggested that enterohaemolysins may enhance the effects of shiga toxins (Caprioli et al., 2005; Holland et al.,

Consumption of gluten is the root cause of the autoimmune response that initiates the cascade of reactions in the body. Gluten proteins can be fractionated into gliadin and glutenin, which are the environmental factors that trigger the immune response in the small intestine.2 These protein molecule complexes are normally unable to permeate the intestinal epithelial. However, with celiac disease, the integrity of tight junctions is compromised, allowing the protein complex to breach the intestinal lining. The regulatory intestinal peptide zonulin is thought to be responsible for the weakened state of tight junctions.2