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PubMed1999

Fecal microflora in healthy infants born by different methods of delivery: permanent changes in intestinal flora after cesarean delivery.

BACKGROUND: Newborn infants in modern maternity hospitals are subject to numerous factors that affect normal intestinal colonization--for example, cesarean delivery and antimicrobial agents. To study the duration of the effect of external factors on intestinal colonization, two groups of infants with different delivery methods were investigated. METHODS: The fecal flora of 64 healthy infants was studied prospectively. Thirty-four infants were delivered vaginally, and 30 by cesarean birth with antibiotic prophylaxis administered to their mothers before the delivery. The fecal flora was cultured on nonselective and selective media in infants 3 to 5, 10, 30, 60, and 180 days of age. Gastrointestinal signs were recorded daily by the mothers for 2 months. RESULTS: The fecal colonization of infants born by cesarean delivery was delayed. Bifidobacterium-like bacteria and Lactobacillus-like bacteria colonization rates reached the rates of vaginally delivered infants at 1 month and 10 days, respectively. Infants born by cesarean delivery were significantly less often colonized with bacteria of the Bacteroides fragilis group than were vaginally delivered infants: At 6 months the rates were 36% and 76%, respectively (p=0.009). The occurrence of gastrointestinal signs did not differ between the study groups. CONCLUSIONS: This study shows for the first time that the primary gut flora in infants born by cesarean delivery may be disturbed for up to 6 months after the birth. The clinical relevance of these changes is unknown, and even longer follow-up is needed to establish how long-lasting these alterations of the primary gut flora can be.

Antibiotic Prophylaxis↗
PubMed1976

Cellular immune reactions against common antigen, small intestine, and colon antigen in patients with Crohn's disease, ulcerative colitis, and cirrhosis of the liver.

Patients with ulcerative colitis showed in 71-93%, patients with cirrhosis of the liver in 64-91%, cellular immunity against Common Antigen (CA) and human fetal intestinal antigens as measured by the leucocyte migration test (LMIT). Patients with Crohn's disease exhibited cellular immune reactions to a lesser degree - from these only patients without immunosuppressive therapy differed significantly from normal controls (p less than 0.05). Approximately 30% of patients with Crohn's disease and ulcerative colitis had elevated antibody titers against intestinal antigens and CA. A high percentage of patients in both diseases showed a reciprocal relationship between cellular and humoral immunity. It was concluded that Crohn's disease and ulcerative colitis can be separated in most cases using intestinal antigens and CA in the LMIT. The occurrence of cellular immunity against these antigens cannot be interpreted as being the only pathogenetic principle in these two diseases. It is also concluded that there appears to be only a weak immune tolerance against intestinal antigens. The high percentage of cellular immune reactions in patients with cirrhosis of the liver demonstrates that this group may have an impairment of the physiological elimination of antigens by the liver.

Antibodies↗
PubMed2006

Thiol/disulfide redox status is oxidized in plasma and small intestinal and colonic mucosa of rats with inadequate sulfur amino acid intake.

Low molecular weight thiol/disulfide redox pools are dependent upon extracellular cysteine (Cys) availability. We determined whether dietary sulfur amino acid (SAA) deficiency induces oxidative stress in vivo, as determined by redox state of major thiol/disulfide couples in plasma [Cys/cystine (CySS)] and intestinal mucosa [glutathione (GSH)/glutathione disulfide (GSSG)]. Rats were fed isocaloric, isonitrogenous semipurified diets: either SAA-adequate (control), SAA-deficient, or SAA-supplemented, pair-fed to intake of the SAA-deficient group. Reference rats consumed standard rat food ad libitum. After 7 d, plasma and gut mucosal samples were analyzed for Cys, CySS, GSH and GSSG, and the redox potentials of Cys/CySS and GSH/GSSG were determined. Mean daily food intake in the pair-fed rats was similar (approximately one-half of reference-rat intake). Body weight decreased in all pair-fed groups, but rats fed the SAA-deficient diet lost significantly more body weight. Dietary SAA deficiency decreased GSH concentrations in both plasma and gut mucosa, increased plasma GSSG, and oxidized plasma and gut mucosal GSH/GSSG redox and plasma Cys/CySS redox. SAA supplementation resulted in a more reducing plasma Cys/CySS redox potential. Reference rats exhibited similar tissue and plasma GSH/GSSG redox as rats that ate semipurified SAA-adequate rat food, which provided similar net SAA intake. Our in vivo data show that inadequate dietary SAA intake oxidizes the thiol/disulfide redox status in rat-gut mucosa and plasma. Such oxidation of redox pools is associated with oxidative stress and the onset or progression of several pathological conditions. Thus, dietary SAA deficiency could contribute to the progression of disease by causing an oxidation of these components.

Amino Acids, Sulfur↗
PubMed1994

Human cultured intestinal cells express attachment sites for uropathogenic Escherichia coli bearing adhesins of the Dr adhesin family.

We have recently demonstrated that cultured human intestinal HT-29 and Caco-2 cell lines express receptors for the F1845 fimbrial adhesin harbored by the diarrheagenic C1845 Escherichia coli (Kernéis et al., Infect. Immun. 59 (1991) 4013-4018). This adhesin belongs to a family of adhesins including the Dr hemagglutinin and the afimbrial adhesin AFA-I harbored by uropathogenic E. coli. Here we investigated the cell association of laboratory E. coli strains expressing the Dr hemagglutinin and the afimbrial adhesin AFA-I with human cultured enterocyte-like or mucosecreting cells. We observed that the E. coli strains bearing these adhesins adhere both to human intestinal undifferentiated and differentiated fluid-transporting cells, and to mucus-secreting cells. This result strongly suggests a high capacity of intestinal colonization for the uropathogenic E. coli harboring adhesive factors belonging to the Dr adhesin family. These results further corroborate the intestinal colonization by uropathogenic E. coli of the Dr family related to the fecal-perineal-urethral hypothesis of urinary tract infection pathogenesis.

Adhesins, Escherichia coli↗
PubMed2002

Liganded VDR induces CYP3A4 in small intestinal and colon cancer cells via DR3 and ER6 vitamin D responsive elements.

The nuclear vitamin D receptor (VDR) mediates the effects of 1,25-dihydroxyvitamin D(3) (1,25D(3)) to alter intestinal gene transcription and promote calcium absorption. Because 1,25D(3) also exerts anti-cancer effects, we examined the efficacy of 1,25D(3) to induce cytochrome P450 (CYP) enzymes. Exposure of human colorectal adenocarcinoma cells (HT-29) to 10(-8)M 1,25D(3) resulted in >/=3-fold induction of CYP3A4 mRNA and protein as assessed by RT-PCR and Western blotting, respectively. Six vitamin D responsive element (VDRE)-like sequences in the promoter region of the CYP3A4 gene were then individually tested for their ability to enhance transcription. A canonical DR3-type element in the distal region of the promoter (-7719-GGGTCAgcaAGTTCA-7733), and a proximal, non-classical everted repeat with a spacer of 6 bp (ER6; -169-TGAACTcaaaggAGGTCA-152) were identified as functional VDREs in this CYP gene. These data suggest that 1,25D(3)-dependent, VDR-mediated induction of CYP3A4 may constitute a chemoprotective mechanism for detoxification of enteric xenobiotics and carcinogens.

Calcitriol↗
PubMed1998

Investigation of the roles of toxin-coregulated pili and mannose-sensitive hemagglutinin pili in the pathogenesis of Vibrio cholerae O139 infection.

In this study, adult volunteers were fed tcpA and mshA deletion mutants of V. cholerae O139 strain CVD 112 to determine the role of toxin-coregulated pili (TCP) and mannose-sensitive hemagglutinin (MSHA) in intestinal colonization. Eight of 10 volunteers who received CVD 112 or CVD 112 delta mshA shed the vaccine strains in their stools; the geometric mean peak excretion for both groups was 1.4 x 10(5) CFU/g of stool. In contrast, only one of nine recipients of CVD 112 delta tcpA shed vibrios in his stool (P < 0.01); during the first 24 h after inoculation, 3 x 10(2) CFU/g was recovered from this volunteer. All recipients of CVD 112 and 8 (80%) of the recipients of CVD 112 delta mshA developed at least a fourfold rise in vibriocidal titer after immunization. In contrast, only one (11%) of the nine recipients of CVD 112 delta tcpA developed a fourfold rise in vibriocidal titer (P < 0.01). We conclude that TCP are an important colonization factor of V. cholerae O139 and probably of El Tor V. cholerae O1. In contrast, MSHA does not appear to promote intestinal colonization in humans.

Adult↗
PubMed1983

[Prospective study of the clinical signs, diet, and radiologic changes of the small intestine and the colon in 106 patients with functional intestinal disorders].

A prospective statistical study of clinical symptoms, radiological modifications of the colon and small bowel as judged by a morphometric method and dietary habits was performed in 106 patients who presented with functional intestinal disorders. Four different associations of symptoms and signs were found: a) pain, sometimes heavy, in the left upper quadrant and the ombilical region was associated with morphometric modifications of the small bowel: increased diameter of the upper part, decreased diameter and increased number of folds in the lower part of ileum; b) slight pain of the two upper quadrants and the two flanks was associated with flatulence, and was not correlated with modifications of the radiological aspect of the small bowel and colon; c) constipation and diarrhea were not correlated with any type of morphometric modifications of the colon; d) constipation was significantly correlated with low fiber diet.

Colon↗
PubMed2002

Recent advances in the endoscopic diagnosis and therapy of upper gastrointestinal, small intestinal, and colonic bleeding.

Endoscopy has become the first and primary diagnostic and therapeutic modality in the management of patients with severe gastrointestinal bleeding. Panendoscopy, push enteroscopy, and colonoscopy provide the diagnostic, prognostic, and therapeutic elements to improve patient outcomes and to reduce morbidity and mortality from severe GI hemorrhage. Recent improvements in endoscopic hemostatic techniques and in imaging modalities using wireless capsule endoscopy suggest that diagnostic and therapeutic endoscopy will be even more important in determining patient outcomes in the future.

Blood Vessels↗
PubMed2003

Pharmacokinetics and delivery of the anti-influenza prodrug oseltamivir to the small intestine and colon using site-specific delivery capsules.

This study investigated the site-specific absorption of oseltamivir using targeted delivery and gamma scintigraphy. On four separate occasions, nine healthy male subjects each received a single 150 mg of oseltamivir administered via the Enterion capsule to the stomach, proximal small bowel, distal small bowel and the ascending colon. Pharmacokinetic parameters of oseltamivir and its carboxylate metabolite show that absorption was similar in the proximal and distal small bowel compared to stomach delivery, but reduced from the ascending colon, demonstrating that absorption-rate limited disposition occurred only for the ascending colon. The metabolite-to-parent ratios were minimally reduced. The results support the feasibility of modified-release formulation development whilst confirming the high and consistent oral bioavailability of oseltamivir.

Acetamides↗
PubMed1993

[Lesions of the small intestine and colon in blunt injuries of the abdomen].

Between 1976 and 1991, we observed lesions of the small bowel or colon in 39 patients having sustained blunt abdominal trauma. 70% of the patients presented with concomitant injuries. Except for 3 cases, all the patients presented with abdominal pain on admission. All the patients were operated on. The delay between admission and operation varied between a few minutes and 48 hours. Indication was hemoperitoneum, peritonitis or progressive abdominal pain. Overall morbidity is high, often related to associated disease. 4 patients died (mortality 10%), including 2 patients with isolated intestinal trauma who were operated on after 20 and 36 hours. Due to the lack of specific laboratory or X-ray test, we suggest a high index of suspicion for bowel lesions in blunt abdominal trauma, especially in unconscious patients. Close observation is mandatory. Indication for laparotomy must not be delayed if any doubt exists regarding the integrity of hollow viscus.

Abdominal Injuries↗
PubMed1995

Endothelial barrier resistance in multiple organs after septic and nonseptic challenges in the rat.

Local variations in endothelial permeability, hypothesized to play a role in the development of multiple-organ injury, were measured by 125I-labeled human serum albumin flux and leakage index in rats with a variety of challenges. The albumin flux significantly increased in the peritoneum, pancreas, stomach, and liver in acute pancreatitis; in the peritoneum and liver in abdominal sepsis; in the spleen, proximal small intestine, colon, liver, lungs, heart, and muscle in bacteremia; in the kidneys, liver, lungs, heart, brain, and muscle in endotoxemia; and in the peritoneum, proximal small intestine, colon, kidneys, liver, and heart after bradykinin administration. A redistribution of the tissue blood content, measured by 51Cr-labeled red blood cells, was noted. An increased albumin leakage index, assaying endothelial permeability considering local hemodynamic alterations, was noted in various organs in the different experimental groups. Thus septic and nonseptic challenges induce endothelial barrier injury. The endothelial resistance appears to be organ and/or tissue dependent and associated with a redistribution of blood.

Abdominal Abscess↗
PubMed1993

Effects of 'contact laxatives' on intestinal and colonic epithelial cell proliferation.

Experimental studies indicate that laxatives may induce epithelial damage. In addition, some laxatives induce the release of prostaglandins. Epithelial cell damage and release of prostaglandins are two pathways by which epithelial cell proliferation could be influenced. Furthermore, fermentable laxatives like lactulose may influence large intestine cell proliferation by the trophic effect of the fermentation products such as short-chain fatty acids. For these reasons an in vivo study in rats was performed to compare the short- and long-term effect of sennosides, bisacodyl, sodium picosulfate and lactulose on epithelial cell proliferation in the ileum and large intestine. Cell proliferation was examined by the BrdUrd labelling technique after 2, 6 and 12 weeks of continuous treatment. Studies in control animals show that the Labeling Index (LI) is higher in the cecum compared with other segments of the colon, and higher in the ileum than in the colon. Treatment with sennosides, bisacodyl and sodium picosulfate does not influence the LI in the ileum and induces no statistically significant increase of the LI when the treated groups are compared with the control group. The proliferative pattern along the crypts remains unchanged with all the laxatives throughout the study. It appears therefore that 'contact' laxatives have no major influence on ileal and colonic epithelial cell proliferation and should not be regarded as tumor-promoting substances.

Animals↗