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PubMed1969

The development of arylsulphatase in the small intestine of the rat.

1. Arylsulphatase activity was measured in stomach, proximal and distal third of small intestine, colon, liver and kidney of foetal and neonatal Sprague-Dawley rats and Swiss mice, with nitrocatechol sulphate as substrate. 2. The specific activity in the distal small intestine, but not in the stomach, proximal small intestine or colon, increased about fourfold between 5 and 16 days after birth in both conventional and germ-free rats. 3. No comparable increase occurred in the distal small intestine of the mouse. 4. The specific activity of acid phosphatase in the distal small intestine of the rat rose only slightly when the arylsulphatase activity increased. 5. The pH optimum and Michaelis constant of arylsulphatase activity of the distal small intestine were similar for 1-day-old, 9-day-old and adult rats. 6. When extracts of distal small intestine of 1-day-old and 9-day-old rats were incubated together, the arylsulphatase activities were additive.

Age Factors↗
PubMed2001

Glycoconjugate metabolism in a cystic fibrosis knockout mouse model.

Cystic fibrosis knockout mice (cftr(-/-)) die prematurely of obstruction of the intestine which may result from accumulation of dehydrated glycoconjugate-containing mucus. We noted an increase in the specific activity of [(14)C]glucosamine-labeled high-molecular weight glycoconjugates, probably mucin, in the lumen of the intestine of cftr(-/-) (homozygous) mice compared to cftr(+/+) (wild-type) and cftr(+/-) (heterozygous) mice and a decrease in the turnover of glycoconjugates of several organs of the cftr(-/-) mice. No difference in the anionic composition of secreted intestinal glycoconjugates was detected and no difference in the amount of mucin 1 (Muc1) was found in the small intestine, colon, pancreas, and lungs of the different genotypes. In addition, the spleen of the cftr(-/-) mice was significantly smaller than that of control mice and the small intestine and colon were, respectively, longer and shorter compared to control mice. These results indicate modified glycoconjugate metabolism in cystic fibrosis knockout mice and morphologic changes to the spleen and intestine where the latter modifications are possibly related to the intestinal malabsorption associated with cystic fibrosis.

Animals↗
PubMed2002

Colonic mucosal vasoactive intestinal peptide receptors in malformations of the enteric nervous system are reduced compared with morphologically normal innervated colon.

Vasoactive intestinal peptide (VIP) is the most important peptidergic transmitter in intestinal relaxation. VIPergic nerves are reduced in aganglionosis (AG). Corresponding findings in intestinal neuronal dysplasia (IND) are sparse. It is unknown whether superficial mucosal VIP receptors are reduced in AG, IND, or hypoganglionosis (HYP) compared to concentrations in morphologically normal innervated colon (MNIC). Cryostat sections from 38 colonic biopsies (23 patients with AG, IND, or HYP, 15 with MNIC) were incubated with radioactive iodinated (125)I-VIP. Receptors were analyzed by autoradiography. Radioactive-marked receptors trigger the precipitation of metallic silver as silver grains within a photographic emulsion. Grains were quantified by image analysis, calculating the percent covered cell surface. Statistical analysis was done by Mann-Whitney and Kruskal-Wallis tests (significance #E5/E5#<0.05). VIP receptors covered 4.31% of the cell surface in MNIC. The values were significantly reduced in AG (2.72%; #E5/E5#=0.012) and IND (2.93%; #E5/E5#=0.008). The two HYP biopsies showed the lowest values (1.83%). Aganglionic colon could be distinguished from healthy proximal segments and IND from habitual constipation. In AG and IND, even the superficial mucosal VIPergic innervation seems to be impaired. The reduction of mucosal VIP receptors in developmental faults of the enteric nervous system may thus be an indicator of a sensomotor disturbance.

Child, Preschool↗
PubMed2003

Framing the future of antifungals in atopic dermatitis.

Atopic dermatitis (AD) is a frequent chronic inflammatory skin disease. Some fungal colonization or infection of the skin may exacerbate AD severity, particularly the so-called head and neck variant. In addition, excessive intestinal colonization by Candida albicans may represent an additional triggering factor. Hence, there is a rationale to use antifungals in selected AD patients. Early trials with topical ketoconazole in head and neck AD showed a decrease in Malassezia colonization, but no significant improvement was observed in the clinical severity. In contrast, clinical improvement and decreased serum IgE were obtained in patients with positive Malassezia radioallergosorbent tests (RASTs) who were treated by oral ketoconazole. Some preliminary data suggested that oral itraconazole treatment in AD patients reduced the need for topical corticosteroids, provided clinical improvement particularly in head and neck AD, reduced the cutaneous and intestinal fungal colonization that may trigger AD, reduced the percentage of positive Malassezia cultures and demonstrated a decrease in C. albicans and Malassezia RAST values. Furthermore, beside its antifungal action, itraconazole in part relieves pruritus and inflammation. In conclusion, oral itraconazole treatment can alleviate AD severity in selected patients. Fluconazole is also effective. Further research is warranted to identify whether the load in skin surface fungal agents, the fungal RAST values and specific prick testing should be assessed in order to optimize the antifungal management in AD patients.

Antifungal Agents↗
PubMed1977

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↗
PubMed1976

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↗
PubMed1985

[Surgical treatment of severe radiation injuries of the small intestine and colon-rectum. Apropos of 85 patients surgically-treated at the Gustave-Roussy Institute].

Radiation lesions of the small intestine, colon and rectum were treated surgically in 85 patients between 1970 and 1983. These were serious complications in all cases involving the short-term vital prognosis in patients lacking signs of recurrence of cancer for which they had received radiotherapy. Immediate operative mortality was 26%. Anastomotic digestive fistulae complicated 31% of resection-anastomosis and 29% of internal bypass operations. During the next 2 years the progression of the chronic radiation lesions themselves required repeat operations due to further complications in 19% of patients, with an operative mortality of 33%. Rather than comparing efficacy of resection-anastomosis with that of internal bypass procedures they should be considered as complementary, since they have different indications. Based on the analysis of results and acquired experience, a surgical strategy is proposed for treating complicated radiation lesions of the intestines.

Adolescent↗
PubMed1989

Age-specific colonization of porcine intestinal epithelium by 987P-piliated enterotoxigenic Escherichia coli.

Neonatal (less than 1-day-old), 3- and 7-day old, and older (3-week-old postweaning) pigs were challenged by intragastric inoculation with 987P-piliated (987P+) enterotoxigenic Escherichia coli (ETEC) 987. Neonatal pigs were colonized (i.e., there were greater than or equal to 10(8) CFU of test strain per 10-cm ileal segment) and developed diarrhea. Intestinal colonization and the incidence and severity of diarrhea were lower in 3- and 7-day old pigs than in neonates. Older pigs were not colonized and did not develop diarrhea following oral inoculation with five strains of 987P+ ETEC. Strain 987 (987P+) adhered in vitro to intestinal epithelial cell brush borders isolated from both neonatal (sensitive) and older (resistant) pigs. The in vivo growth and expression of 987P pilus by strain 987 in ligated ileal loops created in neonatal and older pigs were similar. The in vivo adherence of 987P+ ETEC to intestinal epithelium in ligated ileal loops in neonatal and older pigs was compared. In neonatal pigs, most of the bacteria were in layers associated with the villous epithelium. In older pigs, most of the bacteria were associated with mucus-like material in the intestinal lumen. We concluded that swine develop an innate resistance to 987P+ ETEC by 3 weeks of age. This resistance does not appear to be due to an absence of 987P-specific receptors in the intestines of the older pig or to an inability of 987P+ bacteria to grow and express pili in the older pig. We hypothesized that the resistance of older pigs to 987P-mediated disease is due to release of 987P-specific receptors into the intestinal lumen, where these receptors facilitate bacterial clearance rather than bacterial adherence to intestinal epithelium and colonization.

Aging↗
PubMed1994

Biochemical and genetic analysis of two acetyltransferases from hamster tissues that can metabolize aromatic amine derivatives.

Cytosolic activities in liver, stomach, small intestine, colon, lung, kidney, brain and spleen of hamster have been shown to be capable of N-acetylation, O-acetylation and N,O-acetyltransfer utilizing aromatic amine derivatives as substrates. These activities, which have been implicated in the metabolic activation and carcinogenicity of these compounds, were highest in the liver and small intestine. N-Acetylation could be demonstrated with either acetyl CoA or N-hydroxy-N-acetylaminoarenes serving as acetyl donors. Each of these tissues gave two immunoreactive bands (approximately 29 and 31 kDa) on Western blots using anti-rat AT monoclonal antibodies for detection. Single copies of two distinct acetyltransferase genes, designated AT1 and AT2, were detected in hamster DNA by Southern blot analysis using gene-specific hybridization probes for the 3' end of the AT coding regions. A third gene with > 80% sequence similarity to codons 118-158 of AT2 was also detected. Sequence analysis of the two AT genes showed that both had intronless, 0.87 kb coding regions. One was identical with the AT1 reported by Abu-Zeid et al. (Abu-Zeid,M., Nagata, K., Miyata,M., Ozawa,S., Fukuhara,M. and Yamazoe,Y., 1991, An arylamine acetyltransferase (AT-1) from Syrian golden hamster liver: cloning, complete nucleotide sequence, and expression in mammalian cells. Mol. Carcinogen., 4, 81-88). The second, AT2 (GenBank accession number L24912), coded for a 290 amino acid sequence that was 79% homologous with hamster AT1 and had a calculated molecular weight of 33.8 kDa, a theoretical pI of 5.96 and the three cysteines that have been conserved in all known vertebrate ATs at positions 44, 68 and 223. Northern blot hybridization using gene-specific AT probes detected mRNAs for both AT1 and AT2 in each of the eight tissues analyzed. Two AT1 transcripts, approximately 1.7 and 2.3 kb, were found in approximately equal ratios in all eight tissues. Three transcripts for AT2, approximately 1.9, 2.1 and 2.4 kb, were present in approximately equal ratios in the brain, small intestine, lung and colon. The liver, stomach, kidney and spleen had primarily the smaller two AT2 mRNAs. The overall abundance of AT mRNAs was highest in liver, small intestine and colon. The coding sequences of all AT mRNAs analyzed were identical to their corresponding genes, although the lengths of both the 5' and 3' untranslated transcript regions varied.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetyltransferases↗
PubMed1978

In vitro adhesion of Escherichia coli to porcine small intestinal epithelial cells: pili as adhesive factors.

Escherichia coli strains with pili (K99 or 987P) known to facilitate intestinal colonization adhered in vitro to porcine intestinal epithelial cells. These strains adhered equally to both ileal and jejunal epithelial cells. A laboratory E. coli strain that has type 1 pili also adhered to porcine intestinal epithelial cells. When nonpiliated cells derived from 987P+, K99+, or type 1 pilus+ strains were used for in vitro adhesion assays, they failed to adhere. The attachment of piliated bacteria to epithelial cells was a saturable process that plateaued at 30 to 40 bacterial cells attached per epithelial cell. Competitive inhibition of bacterial cell attachment to epithelial cells with purified pili showed that only purified 987P competed against the 987P+ strain and only purified type 1 pili competed against the type 1 pilus+ strain. Competition between a K99+ strain and K99 was not consistently achieved. K99+, 987P+, and type 1 pilus+ bacteria could be prevented from adhering to epithelial cells by Fab fragments specific for K99, 987P, or type 1 pili, respectively. Fab fragments specific for non-K99 bacterial surface antigens did not inhibit adhesion of the K99+ strain. It is concluded that adhesion of E. coli to porcine intestinal epithelial cells in vitro is mediated by pili and that the epithelial cells used apparently had different receptors for different pili.

Animals↗
PubMed1988

Roles of motility, chemotaxis, and penetration through and growth in intestinal mucus in the ability of an avirulent strain of Salmonella typhimurium to colonize the large intestine of streptomycin-treated mice.

Previously, it had been shown that an avirulent strain of Salmonella typhimurium, SL5316, with wild-type lipopolysaccharide (LPS) was a far better colonizer of the streptomycin-treated CD-1 mouse large intestine, was far more motile, did not bind to mouse intestinal mucus nearly as well as, but penetrated through a layer of intestinal mucus in vitro far better than an almost isogenic LPS-deficient transductant, SL5325. In the present investigation, a nonflagellated transductant, SL5681, and a nonchemotactic transductant, SL5784, were isolated from SL5316 and tested for relative colonizing ability versus SL5316 (smooth) and SL5325 (rough) in streptomycin-treated mice. In addition, the Salmonella strains were tested for their ability to grow together in cecal intestinal mucus and in cecal luminal contents, for their tumbling and swimming activities after growth in cecal mucus, and for their ability to adhere to and travel through cecal mucus in vitro. The data show that the nonflagellated and nonchemotactic derivatives colonized large intestine nearly as well as their parent and were far better colonizers than the LPS-deficient mutant, that all the strains grew equally well in cecal mucus but did not grow in cecal luminal contents, and that cecal mucus-grown strains lost tumbling and swimming activities. Furthermore, the LPS-deficient strain adhered to cecal mucus far better but penetrated mucus far worse than did the nonflagellated transductant, the nonchemotactic transductant, and the parent. Thus, motility and chemotaxis do not appear to play a major role in the ability of the avirulent S. typhimurium strains to colonize the mouse large intestine, colonization may require growth in cecal mucus but does not depend on growth in cecal luminal contents, growth in cecal mucus inhibits S. typhimurium motility, and increased adhesion of the LPS-deficient mutant to cecal mucus and its poor ability to penetrate cecal mucus may play a role in its poor intestine-colonizing ability.

Animals↗
PubMed1995

Cancer incidence in England and Wales and New Zealand and in migrants between the two countries.

Risks of cancer incidence in people born in England and Wales and New Zealand (non-Maoris) living in their home countries, and after migration between the two countries, were analysed using data from their national cancer registries. Since these populations are of similar genetic origin, any real differences in cancer incidence between them are likely to reflect the action of environmental or behavioural risk factors. The greatest differences in risk between the countries were for cutaneous melanoma and lip cancer. In each sex, relative risks of these malignancies were 4 or greater for the New Zealand-born in New Zealand compared with English and Welsh natives in their home country, and risks for migrants in each direction were generally intermediate between those born in the home country in the two countries. Sizeable significantly raised risks in the New Zealand-born in New Zealand compared with English and Welsh natives in England and Wales also occurred for cancers of the mouth, small intestine, colon, thymus, eye and thyroid, and non-Hodgkin's lymphoma in each sex, and for cancer of the prostate. For all of these sites except mouth, small intestine and colon there were also risks around or above New Zealand-born levels for English and Welsh migrants to New Zealand; for colon cancer these migrants had risks close to those in England and Wales. New Zealand migrants to England and Wales had risks of cancers of the colon and prostate that were similar to or above New Zealand levels. Risks of cancers of the stomach, lung, pleura and bladder, and Hodgkin's disease in each sex, and cancers of the cervix, ovary and scrotum and penis, were substantially and significantly lower in the New Zealand-born living in New Zealand than in English and Welsh natives in England and Wales. In English and Welsh migrants to New Zealand risks of bladder cancer in each sex, and of scrotal and penile and pleural cancer in males, approximated to England and Wales risks; cervical cancer risk approximated to the New Zealand risk; and stomach, lung and ovarian cancers showed intermediate risks. Migrants from New Zealand to England and Wales did not gain the lung cancer or clearly the stomach cancer risk of their host country, but did have bladder cancer risks approximating to those in England and Wales.(ABSTRACT TRUNCATED AT 400 WORDS)

Breast Neoplasms↗
PubMed1984

Rocky Mountain spotted fever. Gastrointestinal and pancreatic lesions and rickettsial infection.

Recent clinical studies have shown a high incidence of nausea, vomiting, diarrhea, and abdominal pain in Rocky Mountain spotted fever (RMSF), and case reports have documented rickettsial infection and vascular injury in the small intestine, appendix, and gallbladder. To determine the incidence and distribution of Rickettsia rickettsii and rickettsial lesions that might be the basis for these clinical manifestations of RMSF, tissues that were available from the stomach, small intestine, colon, and pancreas in fatal cases of RMSF were examined. Lesions were identified in pancreatic tissue in 91% of cases and in tissue obtained from the stomach, small intestine, and colon in all cases. Most tissues were judged to be only moderately injured. Organisms of R rickettsii were demonstrated by immunofluorescence in 14 (50%) of 28 cases and, when identified, correlated topographically with the location of vascular injury. These observations support the concept of rickettsial vascular injury of the gastrointestinal (GI) tract and pancreas leading to GI signs and symptoms in RMSF.

Abdomen↗
PubMed2005

Characterizing lipopolysaccharide and core lipid A mutant O1 and O139 Vibrio cholerae strains for adherence properties on mucus-producing cell line HT29-Rev MTX and virulence in mice.

Components of lipopolysaccharide (LPS), i.e. capsule, O antigen, core oligosaccharide, as well as the toxin-coregulated pili are among the factors which significantly contribute to intestinal colonization by Vibrio cholerae O1 and O139. To further address the contribution of LPS to V. cholerae virulence, we performed in vivo colonization experiments and mucus layer attachment studies with defined LPS and capsule mutants of O1 and O139. We investigated the interaction of V. cholerae strains with the differentiated human intestinal cell line HT29-Rev MTX, and found 3-5-fold reduced efficiencies for attachment by defined LPS and capsule mutants of O1 and O139 in comparison with the wild-type strains. In addition, two O1/O139-specific core oligosaccharide biosynthetic gene products, WavJ and WavD, were characterized and tested for colonization. We demonstrate that single and double knockout mutants in wavJ and wavD have an effect on core oligosaccharide biosynthesis, and that these mutants show an attenuated growth in the presence of novobiocin. Curiously, in the mouse intestinal colonization model, only the O139 wavJ,D mutants demonstrated reduced colonization.

Animals↗
PubMed1992

Resistance of severe combined immunodeficient mice to infection with Cryptosporidium parvum: the importance of intestinal microflora.

Cryptosporidium parvum is a protozoan parasite which colonizes intestinal epithelium, causing transient diarrheal illness in immunocompetent hosts and severe chronic disease in immunocompromised hosts. We examined the resistance of severe combined immunodeficient mice, either bearing intestinal flora or germfree, to intestinal infection with C. parvum. Infection was not readily detected in flora-bearing adult severe combined immunodeficient mice until 5 to 7 weeks following oral challenge with C. parvum. In contrast, germfree adult severe combined immunodeficient mice were heavily infected 3 weeks following challenge. These data support the hypothesis that resistance of adult mice to C. parvum infection does not require a specific immune response but can be mediated by nonspecific mechanisms associated with the presence of intestinal flora.

Animals↗
PubMed1999

Neonatal colonization of rats induces immunological tolerance to bacterial antigens.

We wanted to investigate the immunological events occurring in rats intestinally colonized from birth (neonatally) or at adult age with an ovalbumin (OVA)-producing Escherichia coli O6K13 strain, carrying type 1 pili. The neonatally colonized animals responded with lower delayed type hypersensitivity (DTH) against OVA and lower levels of IgG antibodies against OVA, O6 lipopolysaccharide (LPS) and type 1 pili compared to age-matched controls. The IgG antibody response against the bystander antigen, human serum albumin (HSA), was lower in the neonatally colonized animals than in the controls co-immunized with HSA and E. coli, indicating a release of suppressive factors induced by the bacterial antigens. The adult colonized animals showed an increased DTH and antibody response against OVA after immunization. They also had high pre-immunization levels of IgG anti-O6 LPS antibodies compared to controls. However, the relative increase in IgG anti-O6 LPS antibody levels after the immunization with dead E. coli was much lower in the adult colonized animals. The present results suggest that neonatal animals develop tolerance against antigen on bacterial colonizers of the intestine. In addition, this tolerance contains components of suppression.

Animals↗
PubMed1985

Immunoperoxidase detection of pancreatic oncofetal antigen in human tissues.

Normal human adult tissues (from the pancreas, stomach, small intestine, colon and rectum), human fetal pancreas and various human tumor tissues were investigated for the expression of pancreatic oncofetal antigen (POA) by the peroxidase-antiperoxidase complex method. The antibody used in this study was raised by immunization of rabbit with POA purified from ascites of a patient with pancreatic cancer; it was the same as in our previous report on enzyme immunoassay for serum POA. POA was localized in the ductal cells of human fetal pancreas and ductal cell type pancreatic cancer tissue. It was hardly seen in acinar cells of human fetal or adult pancreas, or in acinar cell type pancreatic cancer tissue. Several cancer tissues other than the pancreas revealed positive POA-staining but less frequently. POA was also detected in small amounts in the small duct of normal adult pancreas. In other normal human tissues, POA was recognized in deep crypts of the small intestine and colon. These results indicate that POA is present abundantly in immature ductal cells of the pancreas such as in fetal pancreas and pancreatic cancer, and that high serum levels of POA seen in patients with pancreatic cancer and other malignant tumors may originate from these malignant tissues.

Adult↗
PubMed1985

Role of cholera toxin in enteric colonization by Vibrio cholerae O1 in rabbits.

The role of cholera toxin (CT) in mucosal colonization by Vibrio cholerae O1 was studied in rabbits by using toxinogenic V. cholerae and nontoxinogenic (A-B+ or A-B-) recombinant mutants derived from them. After oral inoculation, toxinogenic strains colonized intestinal mucosa significantly more efficiently than did either A-B- or A-B+ mutants; average colonization was increased 1.5- to 30-fold with toxinogenic strains, depending on the inoculum used and the portion of intestine studied. Additionally, colonization by an A-B- mutant was increased to the levels of its toxinogenic parent by coadministration of CT with the inoculum. We conclude that CT contributes significantly to mucosal colonization by V. cholerae and that this effect is not due to an interaction of the CT B subunit with its mucosal receptor. The possibility that this effect contributes to the in vivo selection of hypertoxinogenic variants of V. cholerae is considered.

Animals↗