Amazoniac
Member
Non-immunological defence mechanisms of the gut
"It is generally accepted that humoral and cellular immunity plays a key role in the defence mechanisms of the gut. In addition, the nonimmunological defence system (Table I) represents an important and often first line of defence. It probably affords sufficient protection, at least in people living in developed countries with good hygiene. This could explain observations that infectious bacterial disorders of the gastrointestinal tract are not more frequently observed in patients with humoral and cell mediated immune deficiency.[1] In some instances, patients totally lacking secretory immunoglobulins maintain a perfectly functioning gut."
"The acidity of the stomach, the motility of the intestine, the antibacterial effects of pancreatic enzymes,[3-5] the normal intestinal flora, lysozyme,[6] and the intestinal secretions are all effective antimicrobial factors that contribute to the non-specific host defence system. Furthermore, normal epithelial cell turnover and intestinal motility act together to purge the intestinal tract of harmful micro-organisms."
GASTRIC ACID
"Intestinal factors in the defence mechanisms of the gut"..
EPITHELIAL CELL TURNOVER
INTESTINAL MOTILITY
PANCREATIC JUICE AND BILE
LYSOZYME (do not confuse with lisazyme: messages like this that make her melt)
INTESTINAL PLORA
"It is generally accepted that humoral and cellular immunity plays a key role in the defence mechanisms of the gut. In addition, the nonimmunological defence system (Table I) represents an important and often first line of defence. It probably affords sufficient protection, at least in people living in developed countries with good hygiene. This could explain observations that infectious bacterial disorders of the gastrointestinal tract are not more frequently observed in patients with humoral and cell mediated immune deficiency.[1] In some instances, patients totally lacking secretory immunoglobulins maintain a perfectly functioning gut."
"The acidity of the stomach, the motility of the intestine, the antibacterial effects of pancreatic enzymes,[3-5] the normal intestinal flora, lysozyme,[6] and the intestinal secretions are all effective antimicrobial factors that contribute to the non-specific host defence system. Furthermore, normal epithelial cell turnover and intestinal motility act together to purge the intestinal tract of harmful micro-organisms."
GASTRIC ACID
"The roles of gastric acid in health and disease are manifold. Firstly, it facilitates digestion of dietary nutrients and augments dietary iron and calcium absorption. Secondly, it acts as a major non-immunological defence factor against exogenous pathogenic micro-organisms, and also suppresses colonisation of the proximal bowel by the oropharyngeal and faecal flora.[10-12]"
"There are a number of studies that show the bactericidal activity of gastric juice in the alive. For example, intragastric bacterial counts, which are normally <10 organisms per ml,[14] rise to >105 organisms per ml when acidity is reduced.[15] Neutralisation of acid by pretreatment with 2 g sodium bicarbonate reduced the infective dose of Vibrio cholerae 10000 fold[16,17] in healthy volunteers. Infections with cholera were more likely to occur in dogs if the bacteria were given together with bicarbonate.[18] [..as posted elsewhere] Similarly, the frequency of enteric multiplication of the vaccine strain of Shigella flexneri increases threefold with sodium bicarbonate neutralisation of gastric juice.[19] With Campylobacter jejuni, a higher incidence of illness was observed in a group of healthy volunteers when the organisms were ingested with sodium bicarbonate.[20] The use of H2 receptor antagonists and proton pump inhibitors (omeprazole) leads to increased intragastric bacterial counts.[15-21] The small bowel colonisation after cimetidine therapy is also considered to be related to reduced gastric acidity due to the drug.[22] Gastric alkalisation of critically ill patients with Mylanta II was found to be associated with intragastric bacterial and fungal colonisation.[23]"
"It is known that bacterial, viral, and parasitic infections suppress gastric acid production in man[41-44] and in animals.[45,46] In fact, bacterial infections, including salmonellosis, tuberculosis, and bronchopneumonia, are associated with suppression of histamine stimulated acid secretion.[41,42] Normochlorhydria was restored upon eradication of infection in most of the cases. Recently, H pylory has been associated with hypochlorhydria and gastritis.[47,48]"
"The mechanism of the suppression of acid secretion in infection is not well understood. It has frequently been thought to be related to direct morphological effects of the infection on the gastric mucosa.[45,53,54] On the other hand, suppression of acid secretion was found to be more marked when there was fever," which indicates that fever rather than infection per se may be responsible for suppression. A transient hypochlorhydria has been shown in people kept in a heated cabinet with a rise of body temperature from 370 to 39°C. The hypochlorhydria observed in infection might be modulated through the stress induced release of endogenous prostaglandins (PGE2), which has been found to suppress acid secretion.[56]"
"There is increasing interest in the role of H pylori in the pathogenesis of peptic ulcer and gastritis.[57-59] H pylori is found in 90-100% of patients with duodenal ulcers, 70% with gastric ulcers,[60,61] and 6-31% of children complaining of vomiting and upper abdominal pain.[62] The role of H pylori in these disorders is indicated by the observation that its eradication in ulcer disease reduces the chance of subsequent relapse.[63,64]"
"Hunt et al recently reported the effect of H pylori on acid production, using 14C-aminopyrin uptake by isolated guinea pig parietal cells. H pylori caused a reduction in basal acid secretion of about 80%, and histamine stimulated acid secretion was reduced to 50% within 15 minutes of inoculation with H pylori.[65] There are also reports describing H pylori associated gastric hypochlorhydria in man.[47,48,66] Although a striking association between the presence of H pylori and hypochlorhydria exists, the question of cause and effect is still obscure. In 1983, Marshall, serving as his own volunteer, rendered himself temporarily hypochlorhydric with cimetidine and then swallowed cells of H pylory cultured from a patient with gastritis.
Although gastritis and H pylori were detected in his follow up tissue specimens,[67,68] a definite association of the organism with hypochlorhydria could not be established, as gastric acid secretion before and after challenge was not monitored in that experiment."
"The gastric acid barrier was found to be impaired in malnourished children and in protein depleted experimental animals.[70-72]"
- Niacin (Nicotinic Acid) a Putative Treatment for Hypochlorhydria: Re-analysis of Two Case Reports
"The low pH of the gastric juice (<3.0) is responsible for its bactericidal properties. Exogenous bacteria introduced into the stomach when the pH is less than 3.0 are usually destroyed within 15 minutes.[13] This bactericidal activity is retained up to pH 4.0.""There are a number of studies that show the bactericidal activity of gastric juice in the alive. For example, intragastric bacterial counts, which are normally <10 organisms per ml,[14] rise to >105 organisms per ml when acidity is reduced.[15] Neutralisation of acid by pretreatment with 2 g sodium bicarbonate reduced the infective dose of Vibrio cholerae 10000 fold[16,17] in healthy volunteers. Infections with cholera were more likely to occur in dogs if the bacteria were given together with bicarbonate.[18] [..as posted elsewhere] Similarly, the frequency of enteric multiplication of the vaccine strain of Shigella flexneri increases threefold with sodium bicarbonate neutralisation of gastric juice.[19] With Campylobacter jejuni, a higher incidence of illness was observed in a group of healthy volunteers when the organisms were ingested with sodium bicarbonate.[20] The use of H2 receptor antagonists and proton pump inhibitors (omeprazole) leads to increased intragastric bacterial counts.[15-21] The small bowel colonisation after cimetidine therapy is also considered to be related to reduced gastric acidity due to the drug.[22] Gastric alkalisation of critically ill patients with Mylanta II was found to be associated with intragastric bacterial and fungal colonisation.[23]"
"It is known that bacterial, viral, and parasitic infections suppress gastric acid production in man[41-44] and in animals.[45,46] In fact, bacterial infections, including salmonellosis, tuberculosis, and bronchopneumonia, are associated with suppression of histamine stimulated acid secretion.[41,42] Normochlorhydria was restored upon eradication of infection in most of the cases. Recently, H pylory has been associated with hypochlorhydria and gastritis.[47,48]"
"The mechanism of the suppression of acid secretion in infection is not well understood. It has frequently been thought to be related to direct morphological effects of the infection on the gastric mucosa.[45,53,54] On the other hand, suppression of acid secretion was found to be more marked when there was fever," which indicates that fever rather than infection per se may be responsible for suppression. A transient hypochlorhydria has been shown in people kept in a heated cabinet with a rise of body temperature from 370 to 39°C. The hypochlorhydria observed in infection might be modulated through the stress induced release of endogenous prostaglandins (PGE2), which has been found to suppress acid secretion.[56]"
"There is increasing interest in the role of H pylori in the pathogenesis of peptic ulcer and gastritis.[57-59] H pylori is found in 90-100% of patients with duodenal ulcers, 70% with gastric ulcers,[60,61] and 6-31% of children complaining of vomiting and upper abdominal pain.[62] The role of H pylori in these disorders is indicated by the observation that its eradication in ulcer disease reduces the chance of subsequent relapse.[63,64]"
"Hunt et al recently reported the effect of H pylori on acid production, using 14C-aminopyrin uptake by isolated guinea pig parietal cells. H pylori caused a reduction in basal acid secretion of about 80%, and histamine stimulated acid secretion was reduced to 50% within 15 minutes of inoculation with H pylori.[65] There are also reports describing H pylori associated gastric hypochlorhydria in man.[47,48,66] Although a striking association between the presence of H pylori and hypochlorhydria exists, the question of cause and effect is still obscure. In 1983, Marshall, serving as his own volunteer, rendered himself temporarily hypochlorhydric with cimetidine and then swallowed cells of H pylory cultured from a patient with gastritis.
Although gastritis and H pylori were detected in his follow up tissue specimens,[67,68] a definite association of the organism with hypochlorhydria could not be established, as gastric acid secretion before and after challenge was not monitored in that experiment.""The gastric acid barrier was found to be impaired in malnourished children and in protein depleted experimental animals.[70-72]"
"Intestinal factors in the defence mechanisms of the gut"..
EPITHELIAL CELL TURNOVER
"The mammalian intestine is covered by a universal epithelium that can either absorb or secrete. An increase in the rate of epithelial surface renewal may occur as a result of bacterial, viral, or parasitic infections. The luminal loss of epithelial cells, connective tissue stroma, and lymphocytes with exuded fluid tends to dilute, dissolve, or wash away the various infective agents adhering to the mucosa and between the cells. This loss of intestinal surface cells acts together with interdigestive motor activity (MMC) to cleanse the intestine and thus prevent stasis and bacterial colonisation."
INTESTINAL MOTILITY
"One important host mechanism limiting the proliferation of organisms in the small intestine is gut motility. In humans, the well defined phase III activity of the interdigestive motor complex (MMC) occurs every 84-112 minutes and migrates down the upper intestinal tract with a speed of about 6-8 cm/minute. The caudate moving band of intense contraction during phase III has been called the 'intestinal housekeeper'.[88,89] The contraction moves digestive contents rapidly down the small intestine. At the port of entry, gastric acid destroys most of the organisms from the outside environment. In the upper intestine this 'housekeeper' mechanism gets rid of microorganisms that managed to escape the gastric acid barrier, and thus prevents stagnation and bacterial overgrowth. The other important role of this movement is to maintain an appropriate distribution of the endogenous enteric microflora and to prevent migration of organisms from the colon.[88,90,91]"
"Altered intestinal motility might have adverse effects on the normal ecology of the intestine. In conditions associated with increased motility, a reduction of the normal gut flora could occur." "[..] decreased motility might lead to stasis and create an ideal culture medium for the development of bacterial overgrowth in the small intestine.[90] The presence of such overgrowth in diabetic patients[93] could in fact be related to delayed intestinal motility.[94]"
"On the other hand, motility disturbances have been reported in the small bowel overgrowth syndrome[90,95,96] which may be the result rather than the cause of increased bacterial growth. The mechanism is still not clear. However, humoral factors may play a role."
"Studies in animal models have provided some information, for example that bacterial enterotoxins may produce abnormal patterns of smooth muscle motor activity."
"Altered intestinal motility might have adverse effects on the normal ecology of the intestine. In conditions associated with increased motility, a reduction of the normal gut flora could occur." "[..] decreased motility might lead to stasis and create an ideal culture medium for the development of bacterial overgrowth in the small intestine.[90] The presence of such overgrowth in diabetic patients[93] could in fact be related to delayed intestinal motility.[94]"
"On the other hand, motility disturbances have been reported in the small bowel overgrowth syndrome[90,95,96] which may be the result rather than the cause of increased bacterial growth. The mechanism is still not clear. However, humoral factors may play a role."
"Studies in animal models have provided some information, for example that bacterial enterotoxins may produce abnormal patterns of smooth muscle motor activity."
Search for 'interdigestive sweep bacteria' for more information.
- The control of gut motility
- Human interdigestive and postprandial gastrointestinal motor and gastrointestinal hormone patterns
- The migrating motor complex: control mechanisms and its role in health and disease (!)
- Perturbation of upper gastrointestinal function by cold stress @Astolfo
- The Pathogenesis of Gastrointestinal Bacterial Overgrowth (shun Nordic lands, earn Netherlands)
- Intestinal motility in irritable bowel syndrome: Is IBS a motility disorder?
- Principles Of Human Physiology (1920)
- The control of gut motility
- Human interdigestive and postprandial gastrointestinal motor and gastrointestinal hormone patterns
- The migrating motor complex: control mechanisms and its role in health and disease (!)
- Perturbation of upper gastrointestinal function by cold stress @Astolfo
- The Pathogenesis of Gastrointestinal Bacterial Overgrowth (shun Nordic lands, earn Netherlands)
- Intestinal motility in irritable bowel syndrome: Is IBS a motility disorder?
- Principles Of Human Physiology (1920)
PANCREATIC JUICE AND BILE
"Bassi [and group] demonstrated bacteriostatic properties of pure pancreatic juice (PPJ).[109]" "In his study the minimum inhibitory concentration (MIC) of the antibiotic mezlocillin against E coli was found to be four times less when PPJ was added, suggesting the ability of PPJ to enhance the activity of this antibiotic."
"The association of exocrine pancreatic insufficiency[101] and bacterial overgrowth[110] in the proximal bowel has been observed in children with protein energy malnutrition. The effect of oral pancreatic enzymes on the intestinal flora has also been studied by Gyr et al in protein deficient monkeys.[5] The study demonstrated that pancreatic extracts hastened the restoration of the normal intestinal flora in protein depleted monkeys to their pre-dietary state."
"The association of exocrine pancreatic insufficiency[101] and bacterial overgrowth[110] in the proximal bowel has been observed in children with protein energy malnutrition. The effect of oral pancreatic enzymes on the intestinal flora has also been studied by Gyr et al in protein deficient monkeys.[5] The study demonstrated that pancreatic extracts hastened the restoration of the normal intestinal flora in protein depleted monkeys to their pre-dietary state."
- Antibacterial activity of the pancreatic fluid [! = of Diokine (that is, great) interested]
- Baking Soda Dramatically Increases Antibiotic Effectiveness, Could Help In Sepsis
- Baking Soda Dramatically Increases Antibiotic Effectiveness, Could Help In Sepsis
LYSOZYME (do not confuse with lisazyme: messages like this that make her melt)
"Lysozyme is an enzyme which has been identified in the digestive system in the ductal cells of salivary glands, in the absorbing epithelium of the intestinal tract, and in pancreatic fluid.[115] The enzyme has been reported to increase in activity in a variety of infections. It is well known to lyse bacteria,[116] and might therefore play a role in mucosal defence against invading organisms."
INTESTINAL PLORA
"The role of the normal intestinal flora as an extremely important host defence mechanism is now beginning to be appreciated. In normal situations, an individual's intestinal flora is highly effective in resisting colonisation by potentially pathogenic invaders. The indigenous flora produces a variety of antimicrobial substances, including colicins[118] and short chain fatty acids,[119] which are potentially bactericidal and bacteriostatic and are therefore considered to inhibit the growth of invading organisms."
"The protective role of the intestinal flora in humans is also suggested by the increased frequency of salmonella infections among Swedish tourists who used prophylactic antibiotics compared with those who took no prophylaxis.[121]"
"The endogenous gut flora also play an important role in maintaining the histological structure of the gut. In fact, it has been demonstrated in the germ-free animal that the 'normal' histology of the gut mucosa is determined by the presence of the bacterial flora.[123] Without the resident flora the intestinal wall has been found to be thinner and to contain only few lymphocytes."
"The protective role of the intestinal flora in humans is also suggested by the increased frequency of salmonella infections among Swedish tourists who used prophylactic antibiotics compared with those who took no prophylaxis.[121]"
"The endogenous gut flora also play an important role in maintaining the histological structure of the gut. In fact, it has been demonstrated in the germ-free animal that the 'normal' histology of the gut mucosa is determined by the presence of the bacterial flora.[123] Without the resident flora the intestinal wall has been found to be thinner and to contain only few lymphocytes."
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