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PubMed1989

Genotyping of Pseudomonas aeruginosa sputum and stool isolates from cystic fibrosis patients: evidence for intestinal colonization and spreading into toilets.

Three hundred and fifty-eight stool and 131 sputum specimens from 40 cystic fibrosis (CF) patients and 100 toilet sinks were investigated for occurrence of Pseudomonas aeruginosa; 67% (21/31) of the patients with chronic P. aeruginosa lung infections carried the organism repeatedly in the stool but the organism was found only once in the stools of nine uninfected patients. P. aeruginosa stool carriage was correlated to high P. aeruginosa numbers in patients' sputa. Typing of P. aeruginosa with a DNA probe showed identity of sputum and stool strains. Seven patients repeatedly carried additional stool strains, not found in the sputum, suggesting intestinal colonization. No differences were seen in the clinical state of patients with P. aeruginosa-negative stool samples and patients with positive stool samples. Toilets in households of P. aeruginosa-infected CF patients were significantly more often contaminated with P. aeruginosa (42%) than toilets in households of non-infected CF patients (20%; P less than 0.03). The study shows that P. aeruginosa-infected CF patients may harbour the organisms also in the intestinal tract, and may spread the bacteria into toilets.

Adolescent↗
PubMed1999

Antibodies to the truncated (short) form of 'O' polysaccharides (TFOP) of Vibrio cholerae O139 lipopolysaccharides protect mice against experimental cholera induced by encapsulated O139 strains and such protection is mediated by inhibition of intestinal colonization of vibrios.

An antiserum raised against the lipopolysaccharides (LPS) of an encapsulated Vibrio cholerae O139 strain was shown to induce passive protection against challenge with O139, but not O1, organisms. Subsequent experiments, however, revealed that the purified LPS, obtained by the conventional phenol-water extraction method, contained capsular polysaccharide (CPS) material. Therefore, another antiserum was raised by immunization with electrophoresed gel-cut material containing only the truncated (short) form of 'O' polysaccharides (TFOP) linked to the core of O139 LPS. Anti-TFOP antibodies and their Fab (IgG) fragments induced passive protection against challenge with colonial variants of encapsulated O139 strains and such protection was mediated by inhibition of intestinal colonization. These results suggest that it is possible to engender protection against encapsulated O139 strains by using TFOP material (devoid of CPS) as the immunogen.

Animals↗
PubMed1993

CTX genetic element encodes a site-specific recombination system and an intestinal colonization factor.

In Vibrio cholerae, the genes encoding cholera toxin (ctxAB) are located on a segment of DNA (termed the "core" region) that is flanked by two or more copies of a repeated sequence called RS1. Together these DNA units comprise the CTX genetic element. Evidence presented here suggests that RS1 sequences encode a site-specific recombination system, which allows integration of a suicide plasmid carrying RS1 into an 18-base-pair sequence (attRS1) located on the chromosome of nontoxigenic V. cholerae strains. Strains of V. cholerae with large deletions removing attRS1 and the entire CTX genetic element no longer undergo site-specific recombination with the RS1 sequence. Additionally, these deletion strains show a defect in intestinal colonization. Recombination experiments localize the gene responsible for enhancing colonization to a portion of the core region of the CTX element. The identified gene encodes a peptide that is highly similar in amino acid sequence to the flexible pilin of Aeromonas hydrophila. These results have important implications in the construction of stable, live attenuated cholera vaccines.

Amino Acid Sequence↗
PubMed1992

Antibodies to outer membrane proteins of Vibrio cholerae induce protection by inhibition of intestinal colonization of vibrios.

An antiserum was raised against the outer membrane (OM) preparation of a Vibrio cholerae 01 strain (Classical, Ogawa) and rendered specific for the outer membrane proteins (OMPs) by absorption with its lipopolysaccharide (LPS). The anti-OMP serum showed reactivity against OM preparations of other 01 and non-01 V. cholerae strains in enzyme-linked immunosorbent assay. The antiserum also induced significant protection against V. cholerae challenge in the suckling mouse model. This protection was found to be independent of biotype, serotype as well as serovar of the challenge organism and was demonstrable even at subagglutinating dilutions of antiserum. The Fab (IgG) fragment, prepared from the anti-OMP serum, also induced passive protection in similar experiments. Further studies demonstrated that the anti-OMP serum as well as its Fab (IgG) fragment markedly inhibited the intestinal colonization of a highly colonizing V. cholerae 01 strain A17 (El Tor, Ogawa). These results highlight the importance of V. cholerae OMPs in immunoprophylaxis against cholera.

Animals↗
PubMed1999

Salmonella infection in a commercial line of ducks; experimental studies on virulence, intestinal colonization and immune protection.

Experimental infections of different salmonella serotypes were established in a commercial line of ducks to provide baseline information on which control measures might be based. The ducks were very resistant to systemic infection with Salmonella typhimurium, S. enteritidis and S. gallinarum within 36 h of hatching. This was associated with an inherent inability of the strains to multiply in the reticulo-endothelial system. The resistance was not associated with poor invasiveness or serum sensitivity. Individual strains of S. typhimurium, S. enteritidis, S. heidelberg and S. orion colonized the gut well and were excreted in the faeces for at least 6 weeks by ducks when they were infected orally within 2 days of hatching. The main sites of colonization were the caeca and, to a lesser extent, the crop. Viable counts of each inoculated strain in the caeca remained in excess of 10(6) c.f.u. 3 weeks after infection although the organisms had been cleared from the spleen by this time. Much less excretion occurred when the birds were infected at 3 weeks of age. When infected ducks, which had cleared themselves of infection, were challenged orally with the homologous strain expressing a different genetic marker, very low levels of excretion of the challenge strain were detected when compared with a control group. After infection low titres of circulating lipopolysaccharide-specific IgG antibodies were detected by an ELISA. Intestinal colonization of newly hatched ducks with an aroA strain of S. enteritidis resulted in extensive colonization which exerted an exclusion effect on the parent strain inoculated 24 h later.

Animals↗
PubMed1999

High intake of milk fat inhibits intestinal colonization of Listeria but not of Salmonella in rats.

During fat digestion, fatty acids and monoglycerides are liberated in the gastrointestinal tract. Generally, these lipids are potent inhibitors of gram-positive bacteria in vitro but have less effect on gram-negative microbes. Considering this, we hypothesized that increased intake of bovine milk fat would result in enhanced gastrointestinal killing of Listeria monocytogenes (gram-positive) but have little effect on infection with Salmonella enteritidis (gram-negative) in rats. To test this, rats were fed either low milk fat diets (10% of energy obtained from milk fat, corresponding to 4. 2 g fat/100 g diet) or high milk fat diets (40% of energy obtained from milk fat, corresponding to 19.6 g fat/100 g diet). After adaptation to these diets, rats were orally infected with Listeria or Salmonella. Greater milk fat consumption in Listeria-infected rats diminished intestinal colonization of Listeria (P < 0.05) and reduced diarrhea (P < 0.05). Analysis of gastrointestinal contents showed that killing of Listeria occurred predominantly in the stomach. High milk fat intake significantly augmented this gastric listericidal capacity (P < 0.05) and raised the concentration of medium-chain and saturated long-chain free fatty acids and of monoglycerides of C12:0, C14:0, C16:0, C18:0, and C18:1 in gastric chyme (P < 0.05). Considering the in vitro listericidal capacity of these agents, it was concluded that particularly the free fatty acids C10:0, C12:0 and C14:0 and the monoglycerides of C12:0, C14:0, and C16:0 seem to play a pivotal role in this enhanced Listeria killing. In contrast, Salmonella infection was not affected by milk fat consumption. In conclusion, high milk fat intake results in higher concentrations of gastric bactericidal lipids and thereby protects against Listeria infection but not against Salmonella.

Animals↗
PubMed2004

Intestinal colonization with Candida albicans and mucosal immunity.

AIM: To observe the relationship between intestinal lumen colonization with Candida albicans and mucosal secretory IgA (sIgA). METHODS: A total of 82 specific-pathogen-free mice were divided randomly into control and colonization groups. After Candida albicans were inoculated into specific-pathogen-free mice, the number of Candida albicans adhering to cecum and mucosal membrane was counted. The lymphocyte proliferation in Peyer's patch and in lamina propria was shown by BrdU incorporation, while mucosal sIgA (surface membrane) isotype switch in Peyer's patch was investigated. IgA plasma cells in lamina propria were observed by immunohistochemical staining. Specific IgA antibodies to Candida albicans were measured with ELISA. RESULTS: From d 3 to d 14 after Candida albicans gavaging to mice, the number of Candida albicans colonizing in lumen and adhering to mucosal membrane was sharply reduced. Candida albicans translocation to mesenteric lymph nodes occurred at early time points following gavage administration and disappeared at later time points. Meanwhile, the content of specific IgA was increased obviously. Proliferation and differentiation of lymphocytes in lamina propria were also increased. CONCLUSION: Lymphocytes in lamina propria play an important role in intestinal mucosal immunity of specific-pathogen-free mice when they are first inoculated with Candida albicans. The decreasing number of Candida albicans in intestine is related to the increased level of specific IgA antibodies in the intestinal mucus.

Animals↗
PubMed1997

Dietary calcium inhibits the intestinal colonization and translocation of Salmonella in rats.

BACKGROUND & AIMS: Dietary calcium decreases the cytotoxicity of intestinal contents and intestinal epitheliolysis by precipitating cytotoxic surfactants such as bile acids. A decreased luminal cytotoxicity might not only strengthen the barrier function of the gut mucosa but also reinforce the protective, endogenous microflora. We hypothesized, therefore, that dietary calcium increases the resistance to intestinal infections. METHODS: Rats on a low-, medium-, or high-calcium purified diet were orally infected with a single dose of Salmonella enteritidis. The kinetics of fecal Salmonella excretion was studied to determine the colonization resistance. Intestinal bacterial translocation was quantitated by measuring urinary oxidation products of nitric oxide (NOx) excretion and culturing bacteria from tissues. RESULTS: Compared with the low-calcium group, the medium- and high-calcium diet-fed rats had a substantially improved colonization resistance. Calcium supplementation also reduced translocation of Salmonella, considering the diminished urinary NOx excretion and viable Salmonella counts in the Ileal Peyer's patches and spleen. Dietary calcium decreased the bile acid concentration and cytotoxicity of fecal water. Several indicators of fecal bacterial mass were significantly increased by supplemental calcium. CONCLUSIONS: Dietary calcium improves the colonization resistance and reduces the severity of gut-derived systemic infections, which is probably attributable to its luminal cytoprotective effects.

Animals↗
PubMed2001

Developmental expression of PEPT1 and PEPT2 in rat small intestine, colon, and kidney.

Mammalian peptide transporters (PEPT1 and PEPT2) play a pivotal role in the absorption of small peptides from the intestine and kidney, respectively, and in the disposition and targeting of peptide or mimetic drugs. However, there are few reports on the molecular basis of their regulation, especially in the young. The aim of this study was to determine the developmental expression of intestinal and renal oligopeptide transporters in rats from embryonic to adult ages. Intestinal segments were collected (i.e. duodenum, jejunum, ileum, and colon) along with whole kidney, and their mRNA and protein levels were measured. Expression levels of PEPT1 were maximal 3-5 d after birth in the duodenum, jejunum, and ileum, and then declined rapidly. Expression was increased transiently at d 24, most notably in the ileum. Adult protein levels were approximately 70% of that observed on d 3-5. Significant PEPT1 expression was observed in colon during the first week of life, but levels were undetectable shortly thereafter through adulthood. PEPT1 and PEPT2 expression is less regulated in rat kidney and more pronounced in older animals. Peptide transporters were also present as early as d 20 of fetal life for all tissues tested. These results are unique in providing the developmental expression of peptide transporter mRNA and protein in distinct regions of the small intestine, colon, and kidney in rat. Our findings suggest that intestinal expression of PEPT1 is induced postpartum, possibly by suckling, and again at the time of weaning, and that the colon may participate in peptide transport early in life.

Animals↗
PubMedDate not supplied

Intestinal colonization and antibody response.

Rapid bacterial colonization of the gastrointestinal tract takes place immediately after birth. Only a few of the Escherichia coli strains colonizing the gut of healthy full-term neonates expressed MS pili. On the other hand, most E. coli strains isolated carried MR pili resembling the P-fimbriae which are a known virulence factor for pyelonephritogenic E. coli. The presence of serum antibodies against pili and K antigens of E. coli after vaccination did not influence the capacity of E. coli to colonize and persist in the intestine of experimental animals.

Animals↗
PubMed2004

Antioxidant effects of dehydroepiandrosterone and 7alpha-hydroxy-dehydroepiandrosterone in the rat colon, intestine and liver.

This study examined in healthy male Wistar rats the in vivo antioxidant effect of dehydroepiandrosterone (DHEA) and 7alpha-hydroxy-DHEA administered by intraperitoneal injections (50 mg/kg body weight) for 2 or 7 days. Markers of oxidative damage to lipids (thiobarbituric acid-reacting substances, TBARS) and to proteins (protein carbonyls) were assessed in colon, small intestine, and liver homogenates. DHEA and 7alpha-hydroxy-DHEA caused a decrease in body weight. DHEA treatment significantly increased liver, colon, and small intestine cell weights. After 7 days, DHEA exerted an antioxidant effect in all organs studied. In the colon, oxidative damage protection was accompanied by a goblet cell proliferation and increase in acidic mucus production. After 2 days, the antioxidant effect of 7alpha-hydroxy-DHEA was mainly observed in the liver. Nonprotein sulfhydryl groups (mostly glutathione levels) were altered by DHEA in the liver whereas they remained unchanged after 7alpha-hydroxy-DHEA treatment. The results indicate that in healthy animals, DHEA exerts a protective effect, particularly in the colon, by reducing the tissue susceptibility to oxidation of both lipids and proteins. This effect was not limited to a specific tissue, whereas the metabolite 7alpha-hydroxy-DHEA exerted its antioxidant effect towards the two markers of oxidative damage earlier than DHEA, and mainly in the liver.

Animals↗
PubMed1990

Escherichia coli F-18 makes a streptomycin-treated mouse large intestine colonization factor when grown in nutrient broth containing glucose.

Escherichia coli F-18 FimA-, a type 1 fimbria-less derivative of a normal human fecal isolate, E. coli F-18, has previously been shown to be as good a colonizer of streptomycin-treated mouse large intestine as its parent, suggesting that type 1 fimbriae are not necessary in this process. In this study it was found that when E. coli F-18 FimA- was grown standing overnight at 37 degrees C in nutrient broth, it remained uniformly suspended; however, when grown in nutrient broth containing 1% (wt/wt) D-glucose, it settled to the bottom of culture tubes. Settling was associated with the formation of clumps (microcolonies) of more than 10 cells each. The effect of glucose could be partially reversed by growing E. coli F-18 FimA- in nutrient broth containing 1% D-glucose supplemented with cyclic AMP (greater than or equal to 1 mM). A reduced-settling mutant of E. coli F-18 FimA-, E. coli F-18 FimA- Set-, selected after Tn5 mutagenesis, was found to be a poor colonizer of streptomycin-treated mouse large intestine when fed to mice simultaneously with the parent strain. These results suggest that glucose-induced settling is, at least in part, regulated in a way related to catabolite repression and that the ability of E. coli F-18 FimA- to form microcolonies plays an important role in its ability to colonize streptomycin-treated mouse large intestine.

Animals↗
PubMed2005

The effect of intestinal colonization of germ-free pigs with Escherichia coli on calprotectin levels in plasma, intestinal and bronchoalveolar lavages.

Calprotectin levels were measured by ELISA in plasma, terminal small bowel lavage and bronchoalveolar lavage from 8-day-old germ-free piglets or gnotobiotic piglets 24 h after colonization with one of the following Escherichia coli strains: non-pathogenic O86, probiotic Nissle 1917 or enteropathogenic O55. The concentration of calprotectin in plasma was about 30 ng/ml only in germ-free piglets and piglets associated with non-pathogenic E. coli. Piglets infected with O55 showed a significant increase of plasma calprotectin and the highest mean level of calprotectin in the bronchoalveolar lavage, which was coincident with septicaemia. However, in the lumen of the small intestine, E. coli Nissle 1917 alone elicited a significant increase of the calprotectin level which was confirmed by immunofluorescence and APAAP immunohistochemistry on cryostat sections through the small bowel. The relevance of this finding to the therapeutic effect of E. coli Nissle 1917 in inflammatory bowel disease is discussed.

Animals↗
PubMed1981

Campylobacter fetus ss. Jejuni, a newly recognized enteric pathogen: morphology and intestinal colonization.

Campylobacter fetus ss. jejuni has recently been recognized as a frequent enteric pathogen of man. Although long known as a significant pathogen of domestic animals, little is known regarding mechanisms of colonization and pathogenesis. In an effort to study the colonization and morphology of this organism, we used scanning electron microscopy to examine ilea and colons from mice in which a human isolate of C. fetus ss. jejuni had been inoculated. When inoculated into the ileum of the mice, a transient colonization was observed by 24 hours and had disappeared by 48 hours. Colonization of the colon first appeared at 48 hours and persisted at least three weeks. When inoculated directly into the colon, colonization appeared within 24 hours in the colon and persisted at least 16 days. Severe colonic necrosis and mucosal degeneration were observed in colons only in those mice which were inoculated via the colon. In the infected colons, the C. fetus ss. jejuni organisms were enmeshed in a fibrous network which may play a role in the attachment of bacteria to the mucosal surface. Differences between the morphology of C. fetus ss. jejuni in the mouse model and that found in pure culture were observed and may represent distinct tissue and culture phases of growth.

Animals↗
PubMed1993

Characteristics of Vero cytotoxin producing Escherichia coli associated with intestinal colonization and diarrhea in calves.

Isolates of Escherichia coli which produce Vero cytotoxin (VTEC) were obtained during 1983-1989 from calves raised in 5 north-central states of the USA. All of the calves experienced intestinal epithelial colonization by VTEC, diarrhea or both; twelve of the calves had bloody diarrhea. Twenty one isolates were serogroup O111 and the others were O103, O69, O45, 026, O5, or non-typable (4 isolates). All but one of the isolates hybridized with the CVD419 probe which identifies most VTEC strains. Thirty two isolates hybridized with the VT1 probe, 3 with both the VT1 and VT2 probes, and one with neither probe. The culture filtrate of the VT probe negative isolate was partially neutralized by SLT I monoclonal antibody. For the other isolates, the results of toxin neutralization by anti-SLT I and anti-SLT II monoclonal antibodies corresponded exactly with the VT1 and VT2 probe hybridization results. Three of the strains adhered in a localized manner to HEp-2 cells and Intestine 407 cells.

Animals↗
PubMedDate not supplied

Congenital anomalies of the small intestine, colon, and rectum.

Congenital anomalies of the gastrointestinal tract are a significant cause of morbidity in children and, less frequently, in adults. These abnormalities include developmental obstructive defects of the small intestine, anomalies of the colon, anomalies of rotation and fixation, anorectal anomalies, and intestinal duplications. Neonates with complete high intestinal obstruction do not usually require further radiologic evaluation following radiography, whereas those with complete low obstruction should undergo a contrast material enema examination. An upper gastrointestinal series must be performed in all patients with incomplete intestinal obstruction because management is different in each case. In low intestinal obstruction, ultrasonography (US) may help differentiate between small bowel obstruction and colonic obstruction. In addition, US can help correctly identify meconium ileus and meconium peritonitis and is useful in the diagnosis of enteric duplication cysts. In malrotation and anorectal anomalies, computed tomography (CT) and magnetic resonance (MR) imaging can provide superb anatomic detail and added diagnostic specificity. Intestinal duplications manifest as an abdominal mass at radiography, contrast enema examination, or US. At CT, most duplications manifest as smoothly rounded, fluid-filled cysts or tubular structures with thin, slightly enhancing walls. At MR imaging, the intracystic fluid has heterogeneous signal intensity on T1-weighted images and homogeneous high signal intensity on T2-weighted images. Familiarity with these gastrointestinal abnormalities is essential for correct diagnosis and appropriate management.

Colon↗
PubMed1987

Demonstration of a flagellar antigen shared by a diverse group of spiral-shaped bacteria that colonize intestinal mucus.

Western blot analysis showed that there is little immunological cross-reactivity of the human pathogens Campylobacter jejuni and Campylobacter coli with Campylobacter pyloridis, except for a very strong cross-reaction between the flagellins. This same antigenic cross-reaction was found with two isolates of gram-negative spiral microaerophilic bacteria that are known to colonize the intestinal mucosa of rodents, but not with the flagellins of a number of other motile bacteria. It is proposed that this shared flagellin antigen may be important structurally and functionally.

Animals↗