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PubMedDate not supplied

Peptide T from human immunodeficiency virus envelope does not interact with hepatic, intestinal and colonic vasoactive intestinal peptide (VIP) receptors.

Acquired immunodeficiency syndrome (AIDS) is initiated by the attachment of the human immunodeficiency virus (HIV) to specific target cells. An octapeptide sequence contained within the envelope of HIV, peptide T, mediates the viral binding. Since there is a considerable structural homology between peptide T and VIP, it has been proposed that the VIP receptor may be the naturally occurring protein which provides the corresponding cellular attachment site. In three different models (rat intestinal epithelial cell membranes, rat liver plasma membranes and human colonic cells), we document the lack of interaction between peptide T and the VIP receptor. These observations would also exclude any pathophysiologic effect caused by the crossreactivity of peptide T or its analogues and these VIP receptors.

Adenocarcinoma↗
PubMed1994

Chemotactic response to mucin by Serpulina hyodysenteriae and other porcine spirochetes: potential role in intestinal colonization.

Chemotaxis of porcine spirochetes towards a variety of mucins was measured quantitatively by a capillary method. A chemotaxis buffer consisting of 0.01 M potassium phosphate buffer (pH 7.0) and 0.2 mM L-cysteine hydrochloride was necessary for chemotaxis of spirochetes. The optimum incubation time and incubation temperature were 1 h and 40 degrees C, respectively. The mucin concentration also affected the chemotaxis observed, and a concentration of 1% (wt/vol) was near the optimum. Virulent Serpulina hyodysenteriae strains were chemotactic towards 1% (wt/vol) hog gastric mucin and 1% (wt/vol) porcine colonic mucin but not towards 1% (wt/vol) bovine submaxillary mucin. Virulent S. hyodysenteriae strains were significantly more chemotactic than avirulent strains of S. hyodysenteriae (SA3 and VS1), Serpulina intermedius, and Serpulina innocens. Other spirochetes belonging to the proposed group of spirochetes Anguillina coli were also not chemotactic. Pathogenicity of S. hyodysenteriae strains that cause swine dysentery may, in part, be attributed to their attraction to porcine intestinal mucus.

Animals↗
PubMed1980

Quantitative evidence of intestinal colonization by Clostridium botulinum in four cases of infant botulism.

Infant botulism is an infectious form of a disease heretofore principally known as food-borne intoxication. Previous epidemiologic and laboratory studies have shown that infant botulism results from the ingestion of spores of Clostridium botulinum that subsequently germinate in the infant intestine and produce botulinal toxin. A quantitative study of the fecal microflora of four infants with infant botulism revealed the presence of C. botulinum in numbers as high as 6.0 x 10(8) colony-forming units (cfu)/g. At various times after the onset of illness, the numbers of C. botulinum that were recovered from feces ranged from 10(3) to 10(8) cfu/g and constituted from 0.01% to 3.3% of the total fecal flora. It was concluded that the large numbers of C. botulinum found in patients' feces could occur only as a consequence of in vivo spore germination and outgrowth.

Botulinum Toxins↗
PubMed2000

Intestinal colonization leading to fecal urobilinoid excretion may play a role in the pathogenesis of neonatal jaundice.

BACKGROUND: Neonatal hyperbilirubinemia remains of concern because of the potential danger for the central nervous system. Because urobilinogen is a nontoxic derivative of bilirubin, the current study was conducted to examine the fecal excretion of urobilinoids and bilirubin in healthy newborns and infants, as well as their intestinal bacteria capable of reducing bilirubin, to assess a possible relation to serum bilirubin levels during the first weeks of life. METHODS: Bilirubin pigments, urobilinoids, and porphyrins were measured in stools of infants during the first week (group A, n = 60) and between the second week and the first 6 months of life (group B, n = 64). Microbiologic analysis of stools was performed in selected cases and bilirubin-converting activity of isolated bacteria was determined in vitro. RESULTS: Urobilinoids were detectable in stools of 57% of the neonates at day 5, but not before. However, fecal urobilinoid production on that day was only a fraction of that observed in adults (0.07 vs. 0.7-3.6 mg/kg per day), whereas at week 6 it increased significantly to an average of 0.9 mg/kg per day. Microbiologic analysis of neonatal stools revealed two novel bacterial strains of Clostridium perfringens and Clostridium difficile capable of reducing bilirubin to urobilinoids. CONCLUSIONS: Urobilinoids can be detected in stools of 57% of newborns at day 5 after delivery. However, the urobilinoid production during the first week of life is quantitatively insufficient to contribute significantly to the removal of bilirubin. Enhancement of the microbial conversion of bilirubin could decrease the intestinal concentration of bilirubin and may decrease the degree or enhance the removal of neonatal hyperbilirubinemia.

Bacteria↗
PubMed2002

Synthetic analogues of beta-1,2 oligomannosides prevent intestinal colonization by the pathogenic yeast Candida albicans.

The pathogenic yeast Candida albicans displays at its cell surface beta-1,2 oligomannosides (beta-1,2-Mans). In contrast to the ubiquitous alpha-Mans, beta-1,2-Mans bind to galectin-3, a major endogenous lectin expressed on epithelial cells. The specific role of beta-1,2-Mans in colonization of the gut by C. albicans was assessed in a mouse model. A selected virulent strain of C. albicans (expressing more beta-1,2-Man epitopes) induced more intense and sustained colonization than an avirulent strain (expressing less beta-1,2-Man epitopes). Synthetic (Sigma) beta-and alpha-linked tetramannosides with antigenicities that mimicked the antigenicities of C. albicans-derived oligomannosides were then constructed. Oral administration of Sigmabeta-1,2-Man (30 mg/kg of body weight) prior to inoculation with the virulent strain resulted in almost complete eradication of yeasts from stool samples, whereas administration of Sigmaalpha-Man at the same dose did not. As most cases of human systemic candidiasis are endogenous in origin, this first demonstration that a synthetic analogue of a yeast adhesin can prevent yeast colonization in the gut opens the possibility of new prophylactic strategies.

Animals↗
PubMed1999

rfb mutations in Vibrio cholerae do not affect surface production of toxin-coregulated pili but still inhibit intestinal colonization.

The toxin-coregulated pilus (TCP) of Vibrio cholerae is essential for colonization. It was recently reported that rfb mutations in V. cholerae 569B cause the translocation arrest of the structural subunit of TCP, raising the possibility that the colonization defects of lipopolysaccharide mutants are due to effects on TCP biogenesis. However, an rfbB gene disruption in either V. cholerae O395 or 569B has no apparent effect on surface TCP production as assessed by immunoelectron microscopy and CTX phage transduction, and an rfbD::Tn5lac mutant of O395 also shows no defect in TCP expression. We conclude that the colonization defect associated with rfb mutations is unrelated to defects in TCP assembly.

Animals↗
PubMed1989

Intestinal colonization with Clostridium difficile in infants up to 18 months of age.

The faecal colonization with Clostridium difficile was investigated among 343 infants during their first 18 months of life. Rectal swabs were taken at the ages of 6 days, 6 weeks, 6 months, 11 months and 18 months. About 25% of the children were colonized with Clostridium difficile between 6 days and 6 months of age. The colonization rate decreased to 3% at 18 months of age. The rate of strains producing cytotoxin was low in infants less than 6 months of age, but at that age about half of the strains isolated were toxin-producing. Breast-fed children were significantly less often colonized with Clostridium difficile than were bottle-fed infants, both at 6 weeks of age (21% versus 47%, p less than 0.05) and at 6 months of age (19% versus 39%, p less than 0.001). Colonization with Clostridium difficile at 6 months of age was associated with a greater frequency of diarrhoeal disease between 6 and 11 months of age (27% versus 16%, p less than 0.05). This association was even more pronounced when the bacteria persisted at 11 months of age (54%, p less than 0.01). Antibiotic therapy could not be demonstrated to influence colonization with Clostridium difficile at any age.

Age Factors↗
PubMed1989

Antibiotic treatment and intestinal colonization by Pseudomonas aeruginosa in cancer patients.

To determine whether antibiotic treatment increases the risk of colonization by Pseudomonas aeruginosa, we performed a case-control study comparing antibiotic exposure in cancer patients colonized by P. aeruginosa and in noncolonized controls. Of 88 patients, 76 had been exposed to at least one antibiotic, but colonization was not statistically associated with exposure to any specific antibiotic treatment, administered orally or parenterally, alone or in combination.

Adolescent↗
PubMedDate not supplied

Intestinal colonization and competitive exclusion of Campylobacter fetus subsp. jejuni in young chicks.

Colonization of Campylobacter fetus subsp. jejuni was investigated in monoxenic and holoxenic chicks. In monoxenic chicks, major colonization was found in the crop and ceca, with populations in the ceca consistently reaching 10(9) colony-forming-units/ml of cecal contents over the 28-day test period. Bacteremia was found in most chicks, but no significant gross pathological lesions were detected. In holoxenic chicks, major colonization occurred only in the ceca, and no evidence of bacteremia was detected. Colonization by native gut microflora sharply reduced subsequent colonization by C. fetus subsp. jejuni. The protective mechanism is perhaps the same as that protective against paratyphoid salmonellae and pathogenic strains of Escherichia coli.

Animals↗
PubMed1985

Inhibition of small intestinal colonization of enterotoxigenic Escherichia coli by streptococcus faecium M74 in pigs.

Colonizing and anti E. coli activity of S. faecium M74 was tested by oral inoculation of cesarean derived, colostrum deprived piglets with Streptococcus faecium M74 and subsequently with a heat stable enterotoxin (ST) producing E. coli (O101 : K30 : K99 : NM). Enterotoxin neutralization and co-culture studies were also performed in vitro. Bacterial counts in 10 cm ileal segments, fluorescein antibody stained cryostat sections, as well as 0.5 micron sections from the ilea of the experimental pigs taken 16 hours post exposure to enterotoxic E. coli (ETEC) all indicated that S. faecium M74 could not colonize the ileum of the newborn pigs, in a single high (7 X 10(8) - 3 X 10(10)) dose either in TSB or in milk suspension, in contrast to the ETEC. However, S. faecium given in milk suspension resulted a marked decrease in ileal colonization of ETEC and in weight loss of piglets. In vitro experiments indicated that neither extracellular nor cell-bound products of S. faecium M74 could neutralise ST, but there was a significant reduction of pH in the TSB cultures of S. faecium that was accompanied by a reduction in ETEC counts of the mixed cultures.

Animals↗
PubMed2001

P fimbriae and aerobactin as intestinal colonization factors for Escherichia coli in Pakistani infants.

The carriage rate of a range of virulence genes was compared between resident and transient Escherichia coli strains obtained from the rectal flora of 22 home-delivered Pakistani infants 0-6 months old. Genes for the following virulence factors were assessed using multiplex PCR: P, type 1 and S fimbriae, three P fimbrial adhesin varieties, Dr haemagglutinin, K1 and K5 capsule, haemolysin and aerobactin. The E. coli strains examined here differed from those previously obtained from hosts in Western Europe in a lower prevalence of genes for P, S and type 1 fimbriae, K1 capsule and haemolysin. Nevertheless, genes for P fimbriae, the class II variety of papG adhesin, and aerobactin were significantly more common among resident than transient strains, as previously observed in a Swedish study. The results suggest that P fimbriae and aerobactin, previously implicated as virulence factors for urinary tract infection, might contribute to persistence of E. coli in the normal intestinal microflora.

Adhesins, Bacterial↗