Bacteria colonic mucosa

Although vitamin K is a fat soluble vitamin, only little stores are found in the body which have to be refilled permanently via dietary input. The role of vitamin K derived from bacteria in the colon is controversely discussed, as the concentration of biliary acids for the resorption the fatsoluble vitamin K is very low in the colon. In addition, only diseases of the small intestine lead to a deficit in vitamin K concentration which cannot be restored by K2 production of colonic bacteria. However, watersoluble vitamin Ks can be resorbed by the colonic mucosa. Maybe because of the little stores for vitamin K, the process of vitamin K-dependent carboxylation of proteins is part of a cycle with several steps during which vitamin K normally is regenerated (see Fig. 1) and thus can be used several times. 

Yet when p-carotene is coated with pectin (edible coating), the pectin prevents p-carotene — or other carotenoids as well as fat-soluble compounds — from being absorbed in the upper parts of the small intestine. As a consequence, these coated compoimds can be transported via the chymus to the colon, where the pectin is broken down to short-chain fatty acids by bacteria. These fatty acids play an important role as growth regulators of the colonic mucosa cells. At the same time, the active agents, such as p-carotene, are released and can then be absorbed by the mucosa. 

Dragstedt concluded that these bacteria colonized the damaged mucosa after ulcer formation and proposed that they had migrated up from the alimentary tract. He did not believe that they played a substantial role in the etiology of the disease and did not pursue these studies further, choosing rather to focus on the role of vagal innervation in acid-induced ulceration. 

Thus bile acids, bacteria, food and chromic inflammatory disease could promote intestinal neoplasia by stimulating epithelial cell renewal. Indeed, hyperproliferative changes can be detected in premalignant colonic mucosa, both in rodents exposed to chemical carcinogens and in patients with familial polyposis coil[45,46]. 

The healthy small intestine contains only a small bacterial population, unlike the colon. However, an acute infection of the mucosa by a virus, bacterium or other parasite can reduce its motility, allowing a huge proliferation of the resident bacteria. Absorption of both macro- and micronutrients is impaired, resulting in the disorder known as sprue. Folic acid is particularly poorly absorbed, causing reduced rates of repair of mucosal cells. Hence, the damage persists and worsens to create a vicious circle. Treatment involves administration of an antibiotic to kill the bacteria and folic acid to allow damaged tissue to recover. The clinical presentation includes bulky stools, steatorrhoea (fatty faeces) and weight loss. 

In the area of a gastric or duodenal peptic ulcer, the mucosa has been attacked by digestive juices to such an extent as to expose the subjacent connective tissue layer (submucosa). This self-digestion occurs when the equilibrium between the corrosive hydrochloric acid and acid-neutralizing mucus, which forms a protective cover on the mucosal surface, is shifted in favor of hydrochloric acid. Mucosal damage can be promoted by Helicobacter pylori bacteria that colonize the gastric mucus. 

Osmotic laxative effects are also produced by the polyhydric alcohols, mannitol and sorbitol, which unlike glucose cannot be transported through the intestinal mucosa, as well as by the non-hydrolyzable disaccharide, lactubse. Fermentation of lactulose by colon bacteria results in acidification of bowel contents and microfloral damage. Lactulose is used in hepatic failure in order to prevent bacterial production of ammonia and its subsequent absorption (absorbable NH3 nonabsorbable NH4+), so as to forestall hepatic coma. 

Mechanism of Action Asalicylicacidderivativethat isconvertedtomesalamineinthe colon by bacterial action. Blocks prostaglandin production in bowel mucosa. Therapeutic Effect Reduces colonic inflammation in inflammatory bowel disease. Pharmacokinetics Small amount absorbed. Protein binding 99%. Metabolized by bacteria in the colon. Minimal elimination in urine and feces. Half-life 0.9 hr. 

Mupirocin (Bactroban) inhibits a specific enzyme responsible for tRNA synthesis in susceptible bacteria. This drug is used topically to treat skin infections caused by Staphylococcus aureus or Streptococcus pyogenes. Likewise, mupirocin can be administered by nasal spray to treat local colonization of S. aureus in the nasal mucosa. This idea may be especially helpful in preventing systemic infection in individuals such as health care workers who are exposed to an outbreak of resistant strains of S. aureus. Local/topical administration of this drug is well tolerated, although some irritation of the skin may occur during topical use, and cough and respiratory irritation can occur when mupirocin is administered by nasal spray. 

The gut microflora consist of microorganisms, mainly bacteria, of the gastrointes linal tract. The small intestine of the adult human is about 4.0 m long. The large intestine, or colon, is about one-third this length (1.5 m). Hie colon receives 1.5-2.U liters of water per day, most of which is absorbed- Only lott-200 mi of water is lost in the feces. The colon also absorbs sodium and chloride originating from the diet and from secretions of the small intestine. The lumenal surface of the large intestine secretes mucus, as docs the small intestine. However, the mucosa of the colon contains crypts but lacks villi. 

It has long been known that the presence or absence of CPS correlates in many cases with disease and that bactericidal and opsonic antibodies directed against them protect the host from invasive disease caused by encapsulated bacteria [2]. Antibodies directed against the LPS play also a major role in protection against infection by avoiding bacterial colonization of specific mucosa or organ [3]. 

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