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At least 145 records · Page 8Linked to original sources
PubMed2003

Effects of tylosin on bacterial mucolysis, Clostridium perfringens colonization, and intestinal barrier function in a chick model of necrotic enteritis.

Necrotic enteritis (NE) is a worldwide poultry disease caused by the alpha toxin-producing bacterium Clostridium perfringens. Disease risk factors include concurrent coccidial infection and the dietary use of cereal grains high in nonstarch polysaccharides (NSP), such as wheat, barley, rye, and oats. Outbreaks of NE can be prevented or treated by the use of in-feed antibiotics. However, the current debate regarding the prophylactic use of antibiotics in animal diets necessitates a better understanding of factors that influence intestinal colonization by C. perfringens as well as the pathophysiological consequences of its growth. We report a study with a chick model of NE, which used molecular (16S rRNA gene [16S rDNA]) and culture-based microbiological techniques to investigate the impact of the macrolide antibiotic tylosin phosphate (100 ppm) and a dietary NSP (pectin) on the community structure of the small intestinal microbiota relative to colonization by C. perfringens. The effects of tylosin and pectin on mucolytic activity of the microbiota and C. perfringens colonization and their relationship to pathological indices of NE were of particular interest. The data demonstrate that tylosin reduced the percentage of mucolytic bacteria in general and the concentration of C. perfringens in particular, and these responses correlated in a temporal fashion with a reduction in the occurrence of NE lesions and an improvement in barrier function. The presence of pectin did not significantly affect the variables measured. Thus, it appears that tylosin can control NE through its modulation of C. perfringens colonization and the mucolytic activity of the intestinal microbiota.

Animal Feed↗
PubMed2005

Neonatal antibiotic treatment alters gastrointestinal tract developmental gene expression and intestinal barrier transcriptome.

The postnatal maturation of the gut, partially modulated by bacterial colonization, ends up in the establishment of an efficient barrier to luminal antigens and bacteria. The use of broad-spectrum antibiotics in pediatric practices alters the gut bacterial colonization and, consequently, may impair the maturation of the gut barrier function. To test this hypothesis, suckling Sprague-Dawley rats received a daily intragastric gavage of antibiotic (Clamoxyl; an amoxicillin-based commercial preparation) or saline solution from postnatal day 7 (d7) until d17 or d21. Luminal microbiota composition and global gene expression profile were analyzed on samples from small intestine and colon of each group. The treatment with Clamoxyl resulted in the almost-complete eradication of Lactobacillus in the whole intestine and in a drastic reduction of colonic total aerobic and anaerobic bacteria, in particular Enterobacteriacae and Enterococcus. The global gene expression analysis revealed that Clamoxyl affects the maturation process of 249 and 149 Affymetrix probe sets in the proximal and distal small intestine, respectively, and 163 probe sets in the colon. The expression of genes coding for Paneth cell products (defensins, matrilysin, and phospholipase A2) was significantly downregulated by the Clamoxyl treatment. A significant downregulation of major histocompatibility complex (MHC) class Ib and II genes, involved in antigen presentation, was also observed. Conversely, mast cell proteases expression was upregulated. These results suggest that early treatment with a large-spectrum antibiotic deeply affects the gut barrier function at the suckling-weaning interface, a period during which the gut is challenged by an array of novel food-borne antigens.

Aging↗
PubMed1994

Intestinal barrier failure and the development of the systemic inflammatory response syndrome.

At the present time, terms used to describe the clinical entity of sepsis are used inappropriately and interchangeably. The source and foci of infection are often unidentified, yet it is clear that some form of inflammatory episode is occurring. The following paper seeks to clarify the terminology used to describe 'sepsis' and link this with a non-bacteraemic source of this inflammatory response--the small intestine. The importance of accurately reflecting oxygen extraction and oxygen consumption by cells is addressed and a movement from the current emphasis on haemodynamic measurement to variables which reflect metabolic rate and lactic acidosis is discussed. Issues which are the concern of nurses working in intensive care are examined, in terms of primary prevention and secondary management.

Critical Care↗
PubMed1992

Development of the neonatal rat small intestinal barrier to nonspecific macromolecular absorption. II. Role of dietary corticosterone.

The role of oral corticosterone (C) in the maturation of the neonatal rat jejunal barrier to the absorption of nonspecific macromolecules was evaluated. This was done by adding C to the diet of rat pups weaned at an early age, 17 d, from maternal milk (MM) to either a protein hydrolysate (PH) or soy (S) artificial formula. Both PH and S are known to cause a delay in small intestinal closure to the absorption of a 40-kD glycoprotein tracer, horseradish peroxidase (HRP), on d 21 of age. C was added to PH and S formulas from d 17 to 21 at 0.26 mumol/L (10 micrograms/dL), a level found in the MM of lactating rat dams, or at 10.29 mumol/L (400 micrograms/dL) (PH + 10C, PH + 400C) (S + 10C, S + 400C). Controls consisted of rat pups fed PH or S without C and animals remaining with the dam on MM. The delay in jejunal closure to HRP on d 21 in both PH- and S-fed pups was prevented by C supplementation at both the higher and lower concentrations. Geometric mean (95% confidence intervals) jejunal HRP absorption in PH + 10C pups was 74 (32,167) IU HRP/mL x cm x min, less than in pups fed PH without C [353 (200,615); p less than 0.05] and indistinguishable from HRP absorption in MM-fed animals [111 (79,154)]. HRP absorption in PH + 400C pups [52 (23,115)] was also less than that in animals fed PH without C (p less than 0.01) and indistinguishable from those fed MM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Development of the neonatal rat small intestinal barrier to nonspecific macromolecular absorption: effect of early weaning to artificial diets.

We studied the effect of early weaning from maternal breast milk to artificial diets on rat jejunal absorption of an exogenous 40-kD glycoprotein, horseradish peroxidase (HRP). Rat pups, fed maternal milk (MM) from birth, received one of three diets for the last 4 d before weaning (d 17-21): MM, protein hydrolysate formula (PH), or soy formula (S). Some rats were pretreated on d 14 with intraperitoneal hydrocortisone (5 mg/rat). In MM-fed rat pups, jejunal HRP absorption was markedly higher on d 17 than on d 21. [Geometric means (95% confidence interval) were: d 17, 626.4 (461.3, 850.6) versus d 21, 90.6 (48.2, 170.5) IU HRP/mL x cm x min, p less than 0.01.] By contrast, 21-d-old PH- and S-fed pups maintained elevated absorption of the tracer [PH, 292.3 (177.5, 480.6), p less than 0.05 versus MM pups, S, 340.8 (164.4, 704.8), p less than 0.01 versus MM pups]. Wt-matched control studies indicate that the difference in HRP absorption was not due to the smaller body wt of formula-fed pups. The increased absorption in formula-fed animals was suppressed by hydrocortisone. In S-fed pups, the increased macromolecular absorption appeared, in part, to be the result of diffusion across altered villus absorptive cells. In PH-fed pups, there was no evidence of damage and HRP absorption appeared to occur by vesicle-mediated transport. Delay in the normal maturation of small intestinal "closure" appears to be associated with early weaning to artificial diets. This may lead to increased nonspecific macromolecular permeability that could result in immune-mediated sensitization and food intolerance.

Age Factors↗
PubMed1996

[The effect of a protein concentrate from milk whey and its fractions on the macromolecular permeability of the intestinal barrier in rats with experimental food anaphylaxis].

Rats received dietary supplement of milk whey concentrate (KSP) being manufactured from skimmed milk by addition of apple pectin (Pec), KSP ultrafiltrated fractions and pure Pec during 21 day. A part of animals were sensitized i/p with chicken ovalbumin and finally subjected to systemic anaphylaxis (SA) by i/v antigen challenge. Gastrointestinal barrier macromolecular permeability (MP) for polyethylene glycol 4000 (PEG-4000) was measured by its urinary excretion after an intragastric load. MP increased significantly in nonsensitized rats after feeding with KSP and its high molecular (HM) fraction but not after feeding with low molecular (LM) KSP fraction compared to NaCl fed group. Feeding with Pec dramatically (5-fold) increased permeability. On the contrary the permeability decreased in sensitized rats subjected to SA when fed with KSP, its LM and particularly HM fraction the later group permeability being normalized down to normal value found in nonsensitized animals. It's concluded that KSP whey protein may be recommended for incorporation into specialized foods for patients with impaired gastrointestinal function.

Anaphylaxis↗
PubMed1998

Molecular and cellular mechanisms of invasion of the intestinal barrier by enteric pathogens. The paradigm of Shigella.

The pathogenesis of bacillary dysentery can be studied at different levels of integration of the cellular components that constitute the colonic mucosal barrier. We considered the interaction of Shigella flexneri in three experimental systems that provide complementary information and a scheme of events occurring in human colorectal mucosa as Shigella invasion proceeds. Interaction of S. flexneri with individual epithelial cells shows a series of events in which the bacterium, upon contact with the cell surface, releases a set of Ipa proteins (i.e. invasins) through a specialized, activable, type-III secretory apparatus (i.e. Mxi/Spa). Via a complex signaling process, these invasins cause major rearrangements of the subcortical cytoskeletal network which allow bacterial entry by a macropinocytotic event. Then the bacterium lyses its phagocytotic vacuole and initiates intracytoplasmic movement, due to polar assembly of actin filaments caused by a bacterial surface protein, IcsA. This allows very efficient colonization of the host cell cytoplasm and passage to adjacent cells via protrusions which are engulfed by a cadherin-dependent process. However, when invasive Shigella are deposited on the apical side of polarized monolayers of human colonic cells, they appear unable to invade, indicating that bacteria need to reach the subepithelial area to invade the epithelium. In this system, it has been shown that transepithelial signaling caused by apical bacteria induces adherence and transmigration of basal polymorphonuclears (PMN), thus disrupting the monolayer permeability and facilitating bacterial invasion. LPS accounts for a large part of this transepithelial signalization to PMN. Such a process could account for invasion in intestinal crypts. Finally, models of infection, such as the rabbit ligated intestinal loop show that initial bacterial entry occurs essentially via M cells of the follicular associated epithelium. It then causes apoptosis of macrophages located in the follicular dome, inducing release of IL-1 beta which, in turn, initiates inflammation, leading to destabilization of the epithelial structures as modeled above. These data can now be used to understand the mechanisms of mucosal protection against bacillary dysentery.

Animals↗
PubMed1960

On the size of the toxic particle passing the intestinal barrier in botulism.

On the basis of toxicity assays using partition centrifugation cells it was established that the sedimentation coefficient of type A botulinum toxin appearing in the lymph of orally poisoned rats was 7.9 x 10(-18) cm. per dyne sec. with 95 per cent confidence limits of 4.4 to 11.4 x 10(-13) cm. per dyne sec. This is a significantly lower value than that obtained for crystalline toxin but is well within the range of size for proteins. Exposure of crystalline toxin for 2 hours to digestive processes in a section of the duodenum of living rats did not significantly reduce the sedimentation coefficient of the toxin. The S(20) of crystalline toxin employed in the present study ranged between 12 and 21 with a mean value of 17.9. While it was observed that both botulinum toxin and albumin sedimented from lymph in glycerol gradient tubes to essentially the same level no evidence was developed to indicate association between toxin in lymph and serum albumin. The electrophoretic mobility of toxin in lymph is like that of crystalline toxin and not albumin. Dialysis of toxic lymph against serum albumin does not result in the appearance of toxin in the dialysate.

Animals↗