Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review stresses the importance of the gut as an immunologic organ, and describes those factors in the gut which impede penetration of potentially harmful macromolecules, particularly the secretory IgA system. Because of the immaturity of this gut function in the young infant, breast feeding should be encouraged for the first six to nine months of life whenever possible.
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PMID:Biological and clinical significance of the gut as a barrier to penetration of macromolecules. Practical implications with respect to breast feeding. 78 35

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional immaturity' of the pancreas.
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PMID:Glucose tolerance and insulin release in malnourished rats. 81 69

The differentiation status of epithelial cells in intestinal adaptation remains unclear. To determine whether enterocytes reach optimum maturity following adaptation after 85% shortening of the rat gut by jejunoileal bypass surgery, activities of two brush border enzymatic markers of differentiation, alkaline phosphatase and sucrase, were examined in subpopulations of epithelial cells isolated sequentially from the villus/crypt axis of normal (sham operated) and hyperplastic mucosa. In jejunal villi, adaptational hyperplasia was associated with an increase in total epithelial alkaline phosphatase, but not total sucrase, activity; alkaline phosphatase activity increased most obviously in cells at the 11-50% position (from the tip) on villi. In hyperplastic ileal villi, total alkaline phosphatase activity fell, although sucrase activity did not change significantly. Specific activity (per mg protein) of sucrase on jejunal villus epithelium was reduced by the adaptational changes to bypass; alkaline phosphatase specific activity remained unchanged. In the ileum, despite adaptational changes to bypass, there was no increase in the normally low specific activities of sucrase and alkaline phosphatase. Bypass surgery did not change the major site of expression of either enzyme on jejunal or ileal villi. In conclusion, enzymatic markers of functional differentiation are not all equally affected by adaptational hyperplasia. Hypertrophy of villi and increased cell proliferation seen in jejunum remaining exposed to luminal contents resulted in an increase in the alkaline phosphatase but not the sucrase content. This is not, therefore, the result of a simple immaturity of villus cells. Morphological adaptation in the ileum, however, is not accompanied by adaptation of brush border enzyme markers of differentiation, confirming a functional immaturity of these cells. Strategies for increasing the expression of these markers may have clinical value.
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PMID:Differentiation status of rat enterocytes after intestinal adaptation to jejunoileal bypass. 148 65

Two-colour immunofluorescence staining for intracellular J chain and IgA (or J chain and IgG) was performed on tissue sections of normal human ileal mucosa (eight adult kidney donors), mesenteric lymph nodes (MLN), peripheral lymph nodes, and palatine tonsils. The most prominent J chain positivity was seen for IgA (97.3%) and IgG (81.7%) immunocytes in the ileal lamina propria (LP). Moreover, the proportion of J chain-expressing extrafollicular immunocytes was significantly higher (P less than 0.05) in MLN than in peripheral lymph nodes for the IgA class (58.5% versus 25.6%); the same proportion for the IgG class was 45.9% versus 30.4%. In clinically normal palatine tonsils of adults, extrafollicular J chain expression was much lower than in peripheral lymph nodes; 14.2% for IgA cells and 5.5% for IgG cells. When related to subclass production, J chain expression was found to be higher for IgA2 than for IgA1 cells in all tissues examined (palatine tonsils excluded because of a small number of IgA2 cells), the difference being significant in MLN and ileal LP (P less than 0.05). The J chain positivity tended to be higher for all IgG subclasses in MLN than in peripheral lymph nodes; this difference was significant (P less than 0.05) for IgG2-producing immunocytes. Taking J chain expression as a marker of clonal immaturity, our results may reflect to some extent distribution of newly generated memory B cell clones from gut-associated lymphoid tissue to MLN, peripheral lymph nodes, and palatine tonsils in a strikingly decreasing order.
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PMID:Terminally differentiated human intestinal B cells. J chain expression of IgA and IgG subclass-producing immunocytes in the distal ileum compared with mesenteric and peripheral lymph nodes. 212 37

Mucosal histology, crypt cell proliferation and brush border enzymes were measured in rats with varying degrees of jejunoileal bypass, in order to compare the effect of systemic and luminal factors on adaptive growth and differentiation (brush border enzymes) in small intestinal epithelium. Eighty five percent jejunoileal bypass caused a functional short gut; in intestine remaining in continuity there were significant increases in segmental weight, villus area and crypt depth, compared with sham operated controls and 25% jejunoileal bypass rats. Despite villus cell hyperplasia in 85% bypass rats, mucosal sucrase and alkaline phosphatase fell in jejunum and remained low in ileum, while leucine amino peptidase rose in ileum. There was a significant fall in villus area (p less than 0.01) and crypt cell production (p less than 0.001) in self emptying loops of 25% bypass rats not exposed to luminal contents compared with control segments of sham operated rats. In contrast, self emptying loops of 85% bypass rats were not atrophied despite the much greater distance from luminal nutrients; the villus area (p less than 0.01) and crypt cell production (p less than 0.005) were higher than in 25% bypass rats, and at least as great as in sham operated rats. These results indicate that adaptive hyperplasia has a variable effect on expression of brush border enzymes which might reflect villus cell immaturity. The atrophic effect of diversion of luminal contents can be counteracted by systemic growth factors released as part of the adaptive response; thus systemic growth factors are not dependent on a permissive effect of luminal contents.
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PMID:Systemic factors are trophic in bypassed rat small intestine in the absence of luminal contents. 238 26

To assess the influence of immaturity on the responsiveness of enterocytes to specific pathogens, a dose-response curve for cholera toxin (CT)-induced fluid secretion was determined in the proximal small intestine of rats at 2 and 4 wk of age. The suckling rat was approximately 50 times more sensitive to CT in triggering the secretory response than the weaned rat, when estimated by the medium-effective dose (ED50, 0.8 vs. 38.9 nM). Cortisone, known to promote enterocyte maturation, when injected into suckling rats, decreased host sensitivity approximately 1,000 times. Neither age nor cortisone decreased the receptor binding of 125I-labeled CT to intestinal microvillus membranes. In contrast, cortisone treatment caused a threefold increase in receptor density from 14.5 to 43.0 pmol/mg protein. The enzyme responsible for the sodium pump, Na+-K+-ATPase, showed a threefold increase in activity both after weaning and after a cortisone treatment. These data indicate that the immature gut exhibited an increased host sensitivity to CT stimulation that was not correlated with initial receptor binding but was related to a lowered Na+-K+-ATPase activity, suggesting that an underdeveloped sodium pump may be partially responsible for the high incidence of secretory diarrhea in neonates.
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PMID:Age and cortisone alter host responsiveness to cholera toxin in the developing gut. 253 37

We have examined the mechanisms that prevent the induction of oral tolerance to protein antigens in neonatal mice. Serum collected from adult mice 1 h after feeding ovalbumin (1 mg/g body wt) was adoptively transferred to mice aged 1, 3, and 42 d (40 microL/g body wt). Whereas delayed-type hypersensitivity was significantly suppressed in adult recipients relative to control groups, no suppression of systemic delayed-type hypersensitivity was found in neonatal recipients. In attempts to identify the immunologic deficiency that prevents mature reactivity to protein antigens in neonates, adult splenocytes were transferred intraperitoneally (10(8) cells/recipient) 24 h before a feed of OVA (1 mg/g body wt) to neonates. Significant suppression of their systemic DTH response, but not of their anti-ovalbumin IgG antibody response was observed, indicating that spleen cell transfer only partially confers adult-type reactivity. Similar results were obtained using a second protein antigen, BSA. Our observations suggest that the failure to induce oral tolerance to protein antigens in neonatal mice is not simply due to immature antigen processing by the gut, but probably reflects cellular and/or antigen handling immaturity of the neonatal immune system.
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PMID:Failure to induce oral tolerance to protein antigens in neonatal mice can be corrected by transfer of adult spleen cells. 281 1

Times of first stool passage were studied in 171 infants who weighed less than 1,500 g at birth. Delayed passage (greater than 48 hours) was noted in 20.4% of this group. Significant differences were noted between the delayed and nondelayed groups for gestational age, presence of severe respiratory distress syndrome, and the time of the first enteral feeding. In very low birth weight infants, delay in the passage of the first stool is a common occurrence. This delay is probably due to physiologic immaturity of the motor mechanisms of the gut, lack of triggering effect of enteral feeds on gut hormones, and the presence of severe respiratory distress syndrome, which may singly or in concert adversely affect gastrointestinal motility.
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PMID:Passage of the first stool in very low birth weight infants. 310 45

Passive intestinal permeability in 33 newborn babies was studied using feeds containing lactulose and mannitol. Each marker is thought to pass across the gut wall by a different route; lactulose by a paracellular and mannitol by a transcellular pathway. Neither is metabolised and both are wholly and solely excreted by the kidney; urinary recovery is a measure of the intestinal uptake. Babies born before 34 weeks' gestation exhibited a higher intestinal permeability to lactulose than more mature babies, and all preterm babies showed an appreciable decline in lactulose absorption during the first week of oral feeds. Babies of 34 to 37 weeks' gestation achieved a 'mature' intestinal permeability to lactulose within four days of starting oral feeds. These findings may reflect the immaturity of the gut of the preterm baby rather than a process essential to adaptation to enteral nutrition.
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PMID:Intestinal permeability in the newborn. 642 83

In order to prevent the penetration of intraluminal material such as micro-organisms, food antigens, toxins etc. across the intestinal mucosa, a complex defence mechanism has been developed. This mechanism consists of non-immunological defence with enzymatic detoxification as well as an immunological one. The nature of the immunological defence has been thoroughly elucidated during the past 10-15 years. This mechanism is in man based on a special local immunological resistance, where production of secretory IgA plays the main role. Immunoglobulin producing plasma cells appear relatively late after birth in the lamina propria of the gut mucosa. Therefore a physiological immaturity of the immunological defence during first weeks of life can be anticipated. The role of the immunological defence system in the control of dietary antigen penetration across gut epithelium has been much discussed. Circulating antibodies to cow's milk proteins in small infants after milk ingestion and the almost constant finding of such antibodies in high titre in patients with selective IgA deficiency even without intestinal disease indicate a highly significant function of this local immunity in antigen handling. It has been suggested that the apparently high incidence of food allergy in infancy is due to immaturity of this system. Cow's milk protein induced enteropathy is also strictly bound to this age group.
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PMID:The immune response of the intestinal mucosa to foreign proteins. 696 45


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