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INTRODUCTION: The aim of the study was to determine the effects of pharmacological manipulation of postoperative intestinal motility on the resistance of colonic anastomoses. MATERIALS AND METHODS: Seventy-one Sprague-Dawley rats were divided into three groups: Group 1 (n = 20; colonic anastomosis+1 cc of saline solution subcutaneously, daily); Group 2 (n = 29; colonic anastomosis+1.2 mg/100 g body weight metoclopramide in 1 cc subcutaneously, daily); and Group 3 (n = 22; colonic anastomosis+2 mg/100 g body weight hyoscine N-butyl-bromide in 1 cc subcutaneously, daily). Surviving rats (20 in each group) were sacrificed 4 days after surgery and adhesions were evaluated. Each segment containing an anastomosis was removed and the bursting pressure was determined. RESULTS: The cause of death during the early postoperative period was dehiscence in 8 cases (7 in Group 2 and 1 in Group 3). General adhesion scores in Group 2 were higher than in Group 3 (P = 0.003). The score for adhesions to the anastomosis in Group 1 was higher than in Group 2, but no statistically significant difference was found. Bursting-pressure was significantly lower in Group 2 than in other groups (P = 0.001). In all cases leakage of dye was observed at the anastomosis. CONCLUSION: The use of metoclopramide (a gastrointestinal prokinetic agent) during the early postoperative period was associated with an increase in dehiscence in colonic anastomosis and, when animals survived, there was a significant decrease in anastomotic resistance. Hyoscine (an inhibitor of gastrointestinal motility) did not improve the healing of anastomoses.
The location and abundance of Campylobacter jejuni and Campylobacter lanienae in the intestines of beef cattle were investigated using real-time quantitative PCR in two studies. In an initial study, digesta and tissue samples were obtained along the digestive tract of two beef steers known to shed C. jejuni and C. lanienae (steers A and B). At the time of slaughter, steer B weighed 540 kg, compared to 600 kg for steer A, yet the intestine of steer B (40.5 m) was 36% longer than the intestine of steer A (26.1 m). In total, 323 digesta samples (20-cm intervals) and 998 tissue samples (3.3- to 6.7-cm intervals) were processed. Campylobacter DNA was detected in the digesta and in association with tissues throughout the small and large intestines of both animals. Although C. jejuni and C. lanienae DNA were detected in both animals, only steer A contained substantial quantities of C. jejuni DNA. In both digesta and tissues of steer A, C. jejuni was present in the duodenum and jejunum. Considerable quantities of C. jejuni DNA also were observed in the digesta obtained from the cecum and ascending colon, but minimal DNA was associated with tissues of these regions. In contrast, steer B contained substantial quantities of C. lanienae DNA, and DNA of this bacterium was limited to the large intestine (i.e., the cecum, proximal ascending colon, descending colon, and rectum); the majority of tissue-associated C. lanienae DNA was present in the cecum, descending colon, and rectum. In a second study, the location and abundance of C. jejuni and C. lanienae DNA were confirmed in the intestines of 20 arbitrarily selected beef cattle. DNA of C. jejuni and C. lanienae were detected in the digesta of 57% and 95% of the animals, respectively. C. jejuni associated with intestinal tissues was most abundant in the duodenum, ileum, and rectum. However, one animal contributed disproportionately to the abundance of C. jejuni DNA in the ileum and rectum. C. lanienae was most abundant in the large intestine, and the highest density of DNA of this bacterium was found in the cecum. Therefore, C. jejuni colonized the proximal small intestine of asymptomatic beef cattle, whereas C. lanienae primarily resided in the cecum, descending colon, and rectum. This information could be instrumental in developing efficacious strategies to manage the release of these bacteria from the gastrointestinal tracts of cattle.
We and others have reported the presence of novel progastrin (PG)/gastrin receptors on normal and cancerous intestinal cells. We had earlier reported the presence of 33-36 kDa gastrin-binding proteins on cellular membranes of colon cancer cells. The goal of the current study was to identify the protein(s) in the 33-36 kDa band, and analyse its functional significance. A carbodiimide crosslinker was used for crosslinking radio-labeled gastrins to membrane proteins from gastrin/PG responsive cell lines. Native membrane proteins, crosslinked to the ligand, were solubulized and enriched by >1000-fold, and analysed by surface-enhanced laser desorption/ionization-time of flight-mass spectrometry. The peptide masses were researched against the NCBInr database using the ProFound search engine. Annexin II (ANX II) was identified, and confirmed by matrix-assisted laser desorption/ionization-time of flight-mass spectrometry. As HCT-116 cells express autocrine PG, the in situ association of PG with ANX II was demonstrated in pulldown assays. Direct binding of PG with ANX II was confirmed in an in vitro binding assay. In order to confirm a functional importance of these observations, sense and anti-sense (AS) ANX II RNA-expressing clones of intestinal epithelial (IEC-18) and human colon cancer (HCT-116) cell lines were generated. AS clones demonstrated a significant loss in the growth response to exogenous (IEC-18) and autocrine (HCT-116) PG. We have thus discovered that membrane-associated ANX II binds PG/gastrins, and partially mediates growth factor effects of the peptides.
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The severity of infections caused by Salmonella enterica serovar Typhimurium varies depending on the host species. Numerous virulence genes have been identified in S. Typhimurium, largely from studies in mice, but their roles in infections of other species remain unclear. In the most comprehensive survey of its kind, through the use of signature-tagged mutagenesis of S. Typhimurium we have identified mutants that were unable to colonize calf intestines, mutants unable to colonize chick intestines and mutants unable to colonize both species. The type three secretion systems encoded on Salmonella pathogenicity islands (SPIs) 1 and 2 were required for efficient colonization of cattle. However, disruption of these secretion systems only caused a minor defect in S. Typhimurium colonization of chicks. Transposon insertions in SPI-4 compromised S. Typhimurium colonization of cattle, but not chicks. This is the first data confirming a role for SPI-4 in pathogenesis. We have also been able to ascribe a role in colonization for cell surface polysaccharides, cell envelope proteins, and many 'housekeeping' genes and genes of unknown function. We conclude that S. Typhimurium uses different strategies to colonize calves and chicks. This has major implications for vaccine design.
Colonization of the intestinal tracts of newly hatched chicks with Escherichia coli was attempted by swabbing test organisms onto the air-shell of 19-day-old embryos. Test organisms consisted of two virulent E. coli isolates, one avirulent isolate, and one laboratory-derived mutant of the avirulent isolate carrying a recombinant plasmid coding for Colicin V production. Chicks were cultured weekly for 3 weeks for total E. coli and for the test organisms using selective media. Control chicks were sampled on weeks 1 and 5, and the normal E. coli intestinal microflora were examined for the production of colicins. The two virulent E. coli isolates maintained colonization of the chicks for the 3-week test period, with titers decreasing from 10' to 10'- colony-forming units (CFU)/g of intestine. The avirulent isolate and laboratory mutant did not consistently colonize the intestinal tracts. The majority of intestinal samples taken from the control chicks at 1 and 5 weeks had colicin-producing E. coli that were inhibitory to the test organisms.
Intestinal trefoil factor (ITF) gene expression was detected in five colon cancer cell lines. ITF was synthesized by mucous cells of LIM 1215 and LIM 1863 lines, from which it is secreted constitutively. The ITF mRNA transcript was estimated to be 0.6 kb. In LIM 1215 cells, the expression of ITF was potently and dose-dependently inhibited by short-chain fatty acids (butyrate > propionate > acetate) within 8 h of application. The inhibitory effect of butyrate was ablated by actinomycin D and preceded its effects on differentiation of LIM 1215 cells as indicated by induction of alkaline phosphatase activity and counting of periodic acid-Schiff-positive cells. The human ITF promoter contained an 11-residue consensus sequence with high homology to the butyrate response element of the cyclin D1 gene. Mobility shift assays show specific binding of this response element to nuclear protein extracts of LIM 1215 cells. We conclude that butyrate inhibits ITF expression in colon cancer cells and that this effect may be mediated transcriptionally and independently of its effects on differentiation.
Previously, we isolated two Tn4351-generated mutants of Bacteroides thetaiotaomicron (46-1 and CS3) that were unable to grow either on heparin or on chondroitin sulfate. This phenotype was unexpected, since the heparin and chondroitin sulfate utilization pathways had appeared from earlier studies to be independent of each other. Mutants 46-1 and CS3 were also of interest because both were unable to compete successfully with wild-type B. thetaiotaomicron in the intestinal tracts of germfree mice. Thus, both appeared to have a colonization defect. We have now cloned the chromosomal locus in which the transposon insertions in 46-1 and CS3 occurred. Southern blot analysis showed that the Tn4351 insertions in 46-1 and CS3 were about 100 bp apart. Using complementation and insertional mutagenesis, we localized the region affected by the 46-1 and CS3 insertions to within 2.5 kbp. This DNA segment was sequenced and found to contain a 401-codon open reading frame (ORF1) and the N-terminal segment of a second open reading frame (ORF2), which was downstream of ORF1 and transcribed in the same direction. The deduced amino acid sequence of ORF1 showed significant homology to that of a putative positive regulator of an arylsulfatase gene in Klebsiella aerogenes. ORF2 was at least 381 amino acids long and did not exhibit homology to any proteins in the data bases searched. Transposon insertions in both mutants 46-1 and CS3 disrupted ORF1. The results of insertional mutagenesis and complementation experiments indicated that ORF2 was not essential for growth on chondroitin sulfate or heparin. Thus, the chondroitin sulfate-negative and heparin-negative phenotypes of 46-1 and CS3 appear to be due to the interruption of a regulatory gene encoded by ORF1 and not to a polar effect of the insertions on a downstream gene(s). The gene encoding ORF1 has been designated chuR, for regulation of chondroitin sulfate and heparin utilization. Transcriptional fusion studies showed that the expression of chuR occurred at the same level under inducing and noninducing conditions, in contrast to the regulated expression of structural genes of the chondroitin sulfate utilization system. chuR was not autoregulated, nor was its expression affected by a mutation (46-4) that eliminated the expression of all chondroitin sulfate utilization genes but did not affect the utilization of heparin.
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The isolation of a bacterial flora specifically associated with the colonic mucosa of patients undergoing large-bowel surgery is described. This flora differed from that of faeces in both the numbers and the types of bacteria isolated. The most striking difference was the reduction in the number of anaerobic bacteria isolated from the colonic mucosa. The ratio of anaerobic to aerobic was approximately 1:1 for mucosa compared with 100:1 for faeces.
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INTRODUCTION: The aetiopathogenesis of terminal ileitis is still unknown, as is the cause of its spread to the small and large bowel. The aim of this study was to shed light on these unknown aspects of Crohn's disease. CONCLUSIONS: The lack of patency of the ileal branch of the ileocolic lymphatic collector which causes terminal ileitis, usually in the earlier part of life, is likely to occur in the foetus around the 10th week of pregnancy as a result of a minor abnormality of the physiological regression of the vitelline duct. Excessive atrophy of the lymphatic network seems to occur, also affecting the rudimentary lymphatic vessels in the midgut destined to become the terminal ileum. The terminal ileitis spreads to the large bowel in an increasing percentage of cases and is directly related to duration of the disease, causing first ileitis plus right colitis, and then ileitis plus total colitis (which, however, does not include the rectum). It may also include the jejunum, causing skip lesions. This spread of lesions is not due to any genetic predisposition (that is to say, it is not predetermined in empirical terms), but rather to the extent of the lymphatic obstruction caused by the spread of immunocomplexes via the lymphatic network. This is shown by the fact that secondary lesions of the jejunum and large bowel are also typical of lymphoedema and that their spread is segmentary. In the light of these pathogenetic mechanisms, it is reasonable to assume that the spread of the process from the ileum to the colon might be prevented by prompt surgery during the initial phase of the ileitis. If these views are correct, the traditional subdivision of Crohn's disease forms into ileitis, ileocolitis and solitary colitis should be replaced by a very simple scheme showing the spread of the primary ileitis very often to ileocolitis, first confined to the right colon and then total. We cannot include either solitary colitis (not clearly defined in the literature) or anorectal Crohn's disease (whose forms have yet to be fully acknowledged) in this scheme.
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Vasoactive intestinal polypeptide (VIP) induces intestinal secretion of water and electrolytes in experimental animals and man. We assessed the ability of angiotensin II (AII) and norepinephrine (NE) to block the secretion evoked by VIP, in vivo. Ileal and colonic segments in rats were perfused in situ for two hours with a physiological buffer containing [14C]-PEG-4000 as a volume marker. Saline (0.9% NaCl) was infused intravenously during the first hour and VIP or a combination of VIP plus AII or NE was infused during the second hour. All (0.7 ng/kg/min) alone enhanced water absorption significantly (p less than 0.01) in the ileum and an appreciable, although not a statistically significant, effect was observed in the colon. AII antagonized the secretory effects of VIP in the ileum as well as in the colon. Norepinephrine (5 micrograms/kg/min) also reversed the effect of VIP on the small intestine and colon. Although the mechanism by which AII antagonizes the secretory effects of VIP has not been identified, it is probable that AII promotes absorption, at least in part secondary to release of mucosal NE.
The fastigial influence on intestinal motility was investigated in acute experiments on chloralosed cats. Motility was recorded both from the small and large intestine. Electrical stimulation of the rostral fastigial pole produced, in combination with a blood pressure rise, increased motor activity in ileum and colon while jejunum could respond with either increased on decreased motility. The intestinal responses were neither secondary to changes in intestinal blood flow, nor to baroreceptor reflexes induced by the increased blood pressure. The excitatory responses were not due to increased parasympathetic activity since sectioning of such pathways failed to abolish the responses. Instead, interruption of adrenergic sympathetic discharge, accomplished either by guanethidine or by sectioning of relevant nerves, aid eliminate the responses, indicating that the fastigial effects were mediated by suppression of prevailing adrenergic tone. Noxious stimuli to the abdomen, including laparotomy, inhibit intestinal motility by a reflex increase in adrenergic discharge. It is suggested that fastigial influence on intestinal motility is mainly due to suppression of this reflex.