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Effects of age, ambient temperature, and heat-stable Escherichia coli enterotoxin on intestinal transit in infant mice.

Some interrelationships among age, ambient temperature, intestinal transit, and enterotoxigenic Escherichia coli infection were studied in an infant mouse model. The transit of dye in the small intestine was accelerated during the response to heat-stable E. coli enterotoxin. Transit in the small intestine of normal mice accelerated with increased age (from less than 17 h to 8 days old) and accelerated with increased ambient temperature (from 25 to 37 degrees C). Transit was more rapid in the jejunum than in the ileum throughout the range of experimental conditions studied. E. coli strains that do not produce any of the pili known facilitate intestinal colonization were cleared from the small intestine more rapidly at 37 degrees C than at 25 degrees C. This clearance was thought to be due to accelerated transit at the higher temperature. In contrast, a strain of E. coli that produces K99 (pili previously shown to facilitate intestinal colonization in other species) was not cleared from the small intestine and colonized more intensively at 37 degrees C than at 25 degrees C. Intensified colonization by this strain was thought to be due to increased production of K99 at the higher temperature. It was suggested that sluggish intestinal transit may also be characteristic of the neonates of other species and be one of the factors predisposing them to intestinal colonization by enteropathogens. It was speculated that this predisposition may be enhanced if the neonates are chilled. However, the effect of ambient temperature on intestinal transit in homeothermic neonates such as pigs, calves, and humans may be different from that in mice because neonatal mice are poikilothermic.

Aging

Genomic Characterization of Antimicrobial Resistance and Virulence in ST11 Carbapenem-Resistant Klebsiella Pneumoniae Colonizing the Intestinal Tract of Elderly Inpatients.

BACKGROUND: This study aimed to elucidate the molecular epidemiology and virulence characteristics of ST11 carbapenem-resistant Klebsiella pneumoniae (CRKP) colonizing the intestinal tract of elderly inpatients in the Chongzhou region, providing a basis for controlling the transmission of such resistant bacteria in high-risk populations. METHODS: CRKP strains isolated from the intestines of elderly inpatients in this region between January 2023 and June 2024 were collected. ST11 strains were identified via multilocus sequence typing (MLST). Whole-genome sequencing, antimicrobial susceptibility testing, and string test, serum killing, biofilm formation, capsular polysaccharide quantification were employed to characterize their resistance genes, virulence genes, and molecular typing profiles. RESULTS: Among 58 CRKP isolates, 17 (29.3%) were ST11. ST11-KL64 was the dominant clone (70.6%). All isolates carried the carbapenemase gene bla KPC-2 and exhibited extensive drug resistance, with tigecycline retaining the highest susceptibility (64.7%). The yersiniabactin system genes (ybtS, fyuA, entB) were universally present, whereas the aerobactin gene cluster (iucABCD-iutA) was detected in only 17.6% of isolates. The virulence regulator rmpA2 was incomplete in all carriers. The hypermucoviscosity phenotype was observed in 35.3% of isolates, which correlated with serum resistance in some strains. Biofilm formation was variable. The mortality rate among colonized patients was 35.3%. CONCLUSION: The ST11-KL64 clone is dominant among CRKP strains colonizing the intestinal tract of elderly patients in this region. This clone universally carries the bla KPC-2 gene conferring carbapenem resistance and exhibits a unique virulence gene profile characterized by a low carriage rate of classical hypervirulence markers and an incomplete rmpA2 regulator gene. This finding clarifies the local epidemic status of this clone and underscores the importance of implementing active surveillance and targeted prevention strategies for high-risk populations.

KL64 serotype

Carcinoid tumors of the alimentary tract. II. Angiographic diagnosis of small intestinal and colonic lesions.

The angiographic findings of five small intestinal and two colonic carcinoids are described and illustrated, together with a review of the pertinent literature. It is pointed out that the demonstration of a complex of angiographic findings related to the primary site, mesentery, and liver is highly specific. It helps in the preoperative diagnosis as well as in the localization and stage of development of the gastrointestinal carcinoid. The triad of findings is composed of: (a) faint to moderate staining at the primary site; (b) narrowing, obstruction of the distal mesenteric arcade, cluster of irregular kinked vessels, and encasement in the more central areas of mesentery; and (c) hypervascular liver metastasis. The colonic lesions examined are unique in the literature, and exhibited angiographic findings similar to the small bowel carcinoids.

Adult

beta-Hexosaminidase isoenzymes in tissues, cultured cells, and media from human fetal intestine and colonic adenocarcinoma.

Isoelectric focusing of tissue homogenates revealed a predominance of beta-hexosaminidase B in colonic adenocarcinoma, whereas beta-hexosaminidase A was greater in paired normal-appearing colonic mucosa from the same patients as well as in a specimen of human fetal colonic mucosa. Because of the recognized cellular heterogeneity of these tissues, our studies were extended to an examination of these isoenzymes in 20 cultured epithelial cell lines derived from human fetal intestine and colonic carcinoma as well as the secreted enzymes in their culture media. While the B:A isoenzyme ratio was higher in human cancer cells as compared to fetal cells, some of the cancer cell lines had a greater proportion of the A isoenzyme. Examination of the isoenzyme profiles in the media of these cells revealed a greater B:A ratio whether of fetal or cancer cell origin. These studies parallel the apparent biological differences of neoplastic colonic epithelium occurring in vivo and are reminiscent of reported oncodevelopmental changes in enzymatic properties present in some malignant tissues. The differential stabilities of these two isoenzymes derived from the culture media of both types of cell lines in vitro may limit their value as markers of human colonic neoplasia.

Adenocarcinoma

The postnatal development of the alimentary canal in the opossum. III. Small intestine and colon.

The duodenum of the newborn opossum exhibits a patent lumen containing scattered elongate villi, whereas the distal segments of the small intestine are smaller in diameter and are filled with short immature villi. The muscularis externa through the small intestine consists of a single layer of myoblasts. Interposed between the intestinal lining epithelium and the muscularis externa is an extensive capillary bed that occupies a considerable proportion of the intestinal wall. Additional villi appear to form during the postnatal period as a result of evaginations of the epithelium, together with underlying connective tissue and vasculature, into the intestinal lumen. Intestinal glands are not observed until 8.5cm, and are shallow in depth even in the adult. The epithelium of the entire small intestine is modified for absorption until just prior to weaning. The principal intestinal lining cells show an extensive apical endocytic complex, large supranuclear vacuoles and numerous cytoplasmic inclusions. Intestinal epithelial cells of the colon also appear to be modified for absorption during the first two weeks after birth. Although goblet cells and Paneth cells are present during the suckling period, they do not comprise a significant population in the intestinal epithelium until after weaning. In contrast to the small intestine, goblet cells are numerous in the colon by the ninth postnatal day. The significance of macromolecular absorption and the possibility of passive immunity being transmitted in the opossum during suckling are discussed and related to similar events that occur in the slckling young of several eutherian species. The possible functional significance of two large membranes that develop in the lamina propria of the intestines after weaning also is discussed.

Animals

Comparative intestinal and colonic absorption of [4-14C] cholesterol in the rat.

[4(-14)C] Cholesterol was administered as an aqueous emulsion with triolein and dry non-fat milk either directly into the upper duodenum or into the ileocaecal junction of lymph duct cannulated rats. Lymph flow rates were similar in the two groups of animals. Whereas ca. 53% of the administered tracer dose of cholesterol was absorbed when introduced into the upper small intestine, only 0.06% appeared in lymph when administered into the caecum. Furthermore, less than 0.01% of the administered isotope was detected in urine and blood. The data demonstrate that the large intestine does not contribute significantly to the absorption of exogenous cholesterol in the rat.

Animals

[Pharmacological studies of loperamide, an anti-diarrheal agent. II. Effects on peristalsis of the small intestine and colon in guinea pigs (author's transl)].

Effects of loperamide on peristalsis in the guinea pig intestines were investigated in comparison with those of morphine and atropine. The following results were obtained. The ejection of intraluminal fluid produced by the peristaltic contraction of the isolated ileum was suppressed by loperamide at a concentration of 10(-8) or 2 X 10(-8) g/ml. Peristalsis in the intestinal loop of anesthetized guinea pigs was inhibited by i.v. administration of loperamide at a dose of 0.03 mg/kg. Morphine (0.03 mg/kg i.v.) and atropine (0.05 mg/kg i.v.) also inhibited the peristaltic contraction. The effect of loperamide continued longer than that of morphine. Peristalsis in the colonic loop of anesthetized guinea pigs was inhibited by i.v. administration of loperamide at a dose of 0.01 or 0.03 mg/kg. Morphine (0.1 mg/kg i.v.) and atropine (0.03 mg/kg i.v.) also inhibited the peristaltic contraction of the colonic loop. Loperamide (0.01 or 0.03 mg/kg i.v.) and morphine (0.1 mg/kg i.v.) caused a slight and temporary increase of resting level of intraluminal pressure with inhibition of peristalsis in the colonic loop. These results suggest that loperamide suppresses the peristaltic contraction caused by distension of the intestinal lumen.

Animals

The sites of action of 5-hydroxytryptamine in nerve-muscle preparations from the guinea-pig small intestine and colon.

1 The sites of action of 5-hydroxytryptamine (5-HT) were examined in isolated segments of guinea-pig intestine. Mechanical records were taken from the longitudinal muscle of the ileum and proximal colon and from the circular muscle of the ileum and distal colon.2 In order to examine direct actions of 5-HT, nerve-mediated responses were blocked with tetrodotoxin (0.2 mug/ml). There was a gradient in the responsiveness of the longitudinal muscle of the ileum; in the proximal ileum it was usually unresponsive, whereas in the distal ileum about 30% of the amplitude of contraction was caused by a direct effect on the muscle. In the circular muscle from all parts of the ileum, direct effects on the muscle were weak or absent. In the distal colon, the circular muscle was almost always unresponsive to direct effects of 5-HT even when concentrations of 5-HT as great as 100 mug/ml were used. All direct actions of 5-HT on intestinal muscle were blocked by methysergide (1 mug/ml), which itself did not affect nerve-mediated responses.3 Excitatory cholinergic nerves and excitatory and inhibitory nerves which released unidentified substances were all stimulated by 5-HT. The contractions mediated through cholinergic nerves were blocked by hyoscine (0.6 mug/ml).4 Tachyphylaxis to the action of 5-HT occurred both for effects mediated through nerves and for direct effects on the muscle. Responses returned promptly after 5-HT was washed from the organ bath.5 While 5-HT blocked its own action on neural receptors, it did not antagonize the stimulation of nicotinic receptors on cholinergic neurones by 1-1 dimethyl-4-phenylpiperazinium iodide (DMPP). Moreover, pentolinium markedly reduced contractions caused by DMPP without significantly affecting responses to 5-HT. In contrast, (+)-tubocurarine, another nicotinic receptor antagonist, was effective in reducing contractions caused by 5-HT.6 Phenyldiguanide, which has been reported to antagonize the stimulant action of 5-HT on cholinergic neurones in the mouse small intestine, did not cause any significant reduction in the action of 5-HT on cholinergic neurones in the guinea-pig ileum unless a concentration of 1 mg/ml was used. However, contractions elicited by carbachol and DMPP were antagonized to a similar extent by phenyldiguanide at this concentration. Antagonism of the action of 5-HT at neural receptors by bromolysergic acid and by tryptamine was found but it was not specific, these drugs causing comparable decreases in responses to 5-HT, carbachol and DMPP.7 The present results, which show that 5-HT has little or no direct effect on the circular muscle of the ileum and colon, imply that, if 5-HT is a transmitter in enteric reflexes, it must be released from interneurones.

Animals

In vivo CRISPRi screens reveal Escherichia coli functional adaptations in the mouse gut.

Escherichia coli exhibits remarkable genetic diversity that enables it to adapt to the intestinal environment. Here we establish an in vivo CRISPR interference platform that leverages bacterial gene fitness as a high-resolution functional reporter of E. coli adaptations within mice harbouring a defined minimal microbial community (OligoMM12). The screen revealed that diet profoundly shapes the metabolic landscape of E. coli and the essential gene profile identified cross-feeding interactions. Comparison between a laboratory strain (MG1655), a uropathogenic strain (CFT073) and an adherent-invasive E. coli (AIEC LF82) identified distinct genetic requirements for intestinal colonization, highlighting divergent motility, stress response and respiration strategies. In a host inflammatory environment, we found that AIEC LF82 preferably colonized the small intestine with a mobile genetic element, Gally prophage, playing an important role in modulating fitness. These findings provide a high-resolution genetic atlas of E. coli's functional adaptation and demonstrate the utility of functional genomics to probe the gut environment itself.

Journal Article

Glutathione peroxidase acitvity in intestinal and liver tissues of rats fed various levels of selenium, sulfur and alpha-tocopherol.

The effects of various levels of selenium, alpha-tocopherol and sulfur on glutathione peroxidase (GSH-Px) activity in intestinal and liver tissues were determined in male rats fed corn-soybean or Torula yeast diets. Rats fed corn-soybean diets had greater GSH-Px activity in the small intestine, colon and liver tissues, catalase activity and selenium in the liver, and body weight gains than those fed Torula yeast diets. GSH-Px activity in the small intestine, colon, and liver tissues as well as concentration of selenium in the liver increased with increasing levels of selenium in Torula yeast diets but not with corn-soybean diets. Tocopherol supplementation had no significant effect on GSH-Px activity in rats fed Torula yeast or corn-soybean diets supplemented with selenium. Supplemental sulfur decreased GSH-Px activity in the small intestine tissues and increased activity in colon tissues.

Animal Feed

Colonization of porcine small intestine by Escherichia coli: colonization and adhesion factors of pig enteropathogens that lack K88.

The colonizing and adhesive attributes of enterotoxigenic acapsular and/or nonpiliated mutants from K88-negative enteropathogenic Escherichia coli strains were compared with their capsulated and piliated parents (parents were piliated when grown in vitro and in vivo). Acapsular, nonpiliated mutants from three different colonizing strains of enteropathogenic E. coli lost their ability to colonize the ileum of newborn pigs. Acapsular, piliated and capsular, nonpiliated mutants were derived from one of the parental strains (987), and both mutants lacked the ability to colonize the ileum of pigs. The only mutants available from a fourth strain (431) were acapsular and piliated, and they colonized as well as their parents. These data indicate that both capsule and pili are involved in colonization by strain 987. In contrast, capsule is not required for colonization by strain 431, but pili may be.

Animals

The intestinal mucosal barrier to intact antigenic protein. Difference between colon and small intestine.

The integrity of the normal mature intestinal mucosal barrier to unaltered proteins was evaluated with tritiated bovine albumin in rats. Intact H3-BSA placed into either colon or small intestinal lumen regularly reached the bloodstream in quantities sufficient to be antigenic or toxigenic, although the fraction of H3-BSA absorbed from the colon (0.13 per cent) was significantly smaller than that absorbed from the small intestine (1.7 per cent). These studies support the possibility that uptake of ingested or bacterial antigens from the normal gut may be involved in the pathogenesis of local intestinal and systemic disease in man.

Animals

Giant hypertrophic gastritis of Basenji dogs.

Giant hypertrophic gastritis is a newly recognized disease of adult Baseji dogs similar to Menetrier's disease of man. It is characterized by weight loss, diarrhea, dry coat, pale membranes, anorexia, raised convoluted rugae in the body of the stomach, palpable fluid- and gas-filled intestines, colonic inflammation, and radiographically demonstrable dilated intestinal loops. Laboratory findings include leukocytosis, neutrophilia, low hemoglobin, hypoalbuminemia, hypobetaglobulinemia, hypergammaglobulinemia, decreased serum fatty acids, hypocholesterolemia, indicanuria, low fecal pH, and increased fecal fat and nitrogen. Four dogs studied had gastritis with hypertrophy and diffuse lymphocytosis and plasmacytosis of the small intestine.

Animals

Colonization of porcine intestine by enterotoxigenic Escherichia coli: selection of piliated forms in vivo, adhesion of piliated forms to epithelial cells in vitro, and incidence of a pilus antigen among porcine enteropathogenic E. coli.

In contrast to K88-positive porcine enterotoxigenic Escherichia coli (ETEC), K88-negative porcine ETEC strains did not adhere to isolated intestinal epithelial cells in vitro. However, they did adhere to intestinal epithelium in vivo. Growth of one such ETEC (strain 987) in pig small intestine consistently yielded a greater percentage of piliated cells than did growth in vitro. This increase was demonstrable by electron microscopy, by change in colonial morphology, and by agglutination in specific antisera against the pili of strain 987. In contrast to the stored stock culture (which contained very few piliated cells), richly piliated forms of strain 987 did adhere to isolated intestinal epithelial cells in vitro. A series of porcine E. coli strains was tested for agglutinability in antiserum against the pili of strain 987, and several K88-negative ETEC strains were agglutinated. These data are consistent with the hypothesis that pili facilitate intestinal adhesion and colonization by K88-negative ETEC strains.

Antigens, Bacterial

Colonization of porcine small intestine by Escherichia coli: ileal colonization and adhesion by pig enteropathogens that lack K88 antigen and by some acapsular mutants.

Seven K88-negative porcine enteropathogenic Escherichia coli, representing three different serogroups, caused severe diarrhea and characteristically colonized the ileum, but not the jejunum, of intragastrically exposed newborn pigs. Bacterial counts of intestinal contents and wall, fluorescence, and scanning electron microscopy all suggested that these strains colonized the ileum by adhesion to the villous epithelium. However, in ligated intestinal loops, these enteropathogenic E. coli strains adhered to jejunal epithelium as well as to ileal epithelium. Acapsular (K-) mutants, derived from one of the principal strains, retained their colonizing and adhesive abilities, whereas K- mutants from three other enteropathogenic E. coli strains did not. It is suggested that: (i) these K88-negative enteropathogenic E. coli colonize the ileum by adhesion, and (ii) the adhesion of some K-88-negative strains is mediated by surface factors other than, or in addition to, the polysaccharide K antigen.

Animals