SUMMARY BackgroundFaecal microbial transplant (FMT) for recurrent Clostridium difficile infection (rCDI) is greatly facilitated by frozen stool banks. However, the effect of frozen storage of stool for greater than 2 months on the viability of stool bacteria is unknown and the efficacy of FMT is not clear.

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Substantial amounts of phenols are produced in the human colon by bacterial fermentation of protein. In the colonic mucosa of animals, phenols are inactivated predominantly by conjugation with sulphate. The purpose of this study was to confirm sulphation of phenols by isolated colonocytes from man and to evaluate mucosal sulphation in inflammatory bowel disease using the phenol, paracetamol, in rectal dialysis bags. The incubation of paracetamol with colonocytes isolated from resected colon specimens (n=7) yielded a mean (SE) value of 7 0 (0.9) ,tmol/g dry weight of paracetamol sulphate after 60 minutes but virtually undetectable values of paracetamol glucuronide. Paracetamol sulphate was detected in rectal dialysates from all control subjects, with a mean (SE) value of 4-2 (0.8) nmol/hour. Sulphation was significantly impaired (p<0-01) in 19 patients with active ulcerative colitis (0.6 (0 2) nmol/hour) and in 17 patients with ulcerative colitis in remission (1-1 (0-4) nmol/hour). Sulphation in eight patients with Crohn's colitis (4.3 (2.1) nmol/hour) was similar to that in control subjects. Impairment of the capacity of the mucosa to sulphate phenols in quiescent and active ulcerative colitis may pose a metabolic burden on colonic epithelial cells, which are continuously exposed to endogenous phenols from the colonic lumen. The fermentation of protein by bacteria from the human colon generates considerable amounts of phenols and phenylated short chain fatty acids such as phenyl propionate and hydroxyphenyl acetate. ' Some of these volatile phenols may have adverse effects on colonocytes and harmful effects elsewhere in the body.23 In the intact human colon, the concentration of phenols increases progressively from the caecum to the left colon, with maximal concentrations (2 0-3 0 mmol/kg) in the rectosigmoid region.45 Studies in vitro suggest that higher concentrations could be reached under optimal fermentation conditions.6 Although the functional effect of these endogenous phenols remains unclear, the use of an exogenous phenol (paracetamol) has been associated with the onset of exacerbations of ulcerative colitis.7In experimental animals, the inactivation of phenols by the colonic mucosa is mainly achieved by conjugation with sulphate.89 This also seems likely in humans,'0 although studies using colonocytes from resected colon specimens have not been undertaken. The purpose of this study was to examine the sulphation of paracetamol by human colonocytes and to evaluate the sulphation of phenols in inflammatory bowel disease using paracetamol in rectal dialysis bags. Patients and methods STUDIES WITH HUMAN COLONOCYTESColonocytes were isolated from the unaffected mucosa (at least 10 cm from the tumour) of seven colon specimens resected for colonic cancer. Five specimens were from the descending colon and two from the ascending colon. Colonocytes were prepared by mechanical dissociation after incubation in a divalent calcium free solution containing ethylenediaminetetra acetic acid (EDTA

Summary After oral administration of cysts of the intestinal protozoan parasite, Giardia muris, young male C3H/He mice are chronically infected, whereas BALB/c mice demonstrate a rapidly resolving pattern of infection. Both strains of mice injected with trophozoites in adjuvant and challenged orally with cysts develop serum antibodies to numerous trophozoite proteins. A limited number of these protein antigens was differenliatly immunoprecipitated by sera from resistant BALB/c and susceptible C3H/He mice exposed to G. muris. 35S‐methionine‐labelled protein antigens better recognized by immune BALB/c sera included molecules of relative mobility (Mr) 82,000 and a series of proteins of Mr 25,000 to 32,000, Differential recognition extended to a subset of solubilized trophozoite antigens that bind to the Iectin. wheat germ agglutinin (WGA), and that can be radio‐iodinated. In particular, a complex of 4 acidic protein antigens of approximate Mr 32,000. and designated collectively as Gm32, was better recognized by immune BALB/c serum than C3H/He serum. Isolated WGA‐binding antigens were not able to consistently vaccinate BALB/c mice against subsequent G. muris infection. Moreover, preliminary evidence has been obtained that lack of antibody responsiveness to Gm32 does not segregate strictly with susceptibility to chronic infection in (BALB/c × C3H/He)F2 mice. These data, plus the observation that drug‐cured C3H/He mice are highly resistant to reinfection, has led to examination of whether mice differ in the capacity of the intestines to support inflammatory responses. Mast cell deficient Wf/Wf mice, unlike wild‐type litter‐mates, developed chronic giardiasis although no reconstitution of resistance has yet been achieved with inocula of bone marrow cells from +/+ mice. BALB/c mice injected with the antihistamine and antiserotonin drug, cyproheptadine, also showed prolonged infections with G. muris. The data suggest that analysis of specificity differences in immune responses of mice varying in susceptibility to intestinal parasites must be supplemented by examination of the capacity of the intestine to support induced immune responses.

The effect of cholera toxin (CT) and Escherichia coli heat-stable enterotoxin (ST) on the ileum and colon was examined in vivo in the rat in an attempt to clarify the effects of enterotoxins on colonic mucosa and to determine if these effects were influenced by short-chain fatty acids (SCFA). Both CT and ST induced similar changes in water and electrolyte fluxes, and the magnitude of these changes in loops of colon was similar to that observed in loops of ileum. The addition of luminal SCFA, acetate, propionate and butyrate did not influence the effect of either toxin in loops of ileum. However, in loops of colon exposed to CT, luminal butyrate (40 mM) largely reversed the effect of CT by converting net water secretion (mean ± SE, -363 ± 154 nl•cm^-2•min^-1) to net water absorption (470 ± 194 nl·cm^-2·min^-1) and by significantly reducing the net secretion of sodium ions. In loops of colon exposed to ST, similar effects were observed although net water secretion (-784 ± 114 nl•cm^-2•min^-1) was only partially reversed by butyrate (-318 ± 102 nl•cm^-2•min^-1). In contrast to butyrate, acetate and propionate did not influence changes in colonic fluxes of water and sodium induced by enterotoxins. Oxidation of butyrate and glucose was observed to be depressed in colonocytes pre-exposed to CT but not to ST. In this model, colonic secretion induced by enterotoxins is similar to that observed in the ileum but differs from ileal secretion in its modulation by luminal butyrate.

SUMMARY Conjugation of phenol by the colonic mucosa was assessed in vivo using dialysis tubing containing 15 ml of 1 mmol/l acetaminophen (paracetamol) and 10 mmol/l butyrate. These were allowed to equilibrate in the rectum for one hour. The glucuronidated and sulphated conjugates of acetaminophen were measured by high pressure liquid chromatography and bicarbonate concentrations by gas analysis. In 21 subjects without colonic disease sulphate conjugation was observed in all cases, with a mean (SE) of 3-86 (0-66) nmol/hour, while glucuronide conjugation was found in seven of 21 cases. Mean (SE) bicarbonate output of42 9 (3 9) ,mol/hour (n = 21) indicated healthy colonic mucosal metabolism and phenolic sulphation in dialysate and agreed with published sulphation rates obtained with cultured cells of colonic epithelium.Acetaminophen sulphation suggests that the colonic mucosa has an important role in the conjugation of phenols, and the method reported here would be useful in assessing the detoxification capacity of the colonic mucosa in diseases of the rectal mucosa.Relatively little attention has been directed towards the capacity of the colonic mucosa to inactivate dietary or bacterial phenols. Self

Results from endoscopic sphincter of Oddi manometry are being used to support the diagnosis of sphincter dysfunction in patients with unexplained pain after cholecystectomy. However, there are few data on the reproducibility of manometric records or motility diagnosis during a second test. In this study, the reproducibility of manometric records was assessed in 12 patients with pain after cholecystectomy by performing a second study after three months. Manometric tracings were evaluated without access to patients details and scored for sphincter basal pressure, frequency and amplitude of phasic contractions, propagation of phasic contractions, and responses to intravenous injection of cholecystokinin octapeptide (20 ng/kg). At the initial manometric study, four patients were diagnosed as normal, four as stenotic, and four as dyskinetic. Those diagnosed as normal and stenotic at the first study had an identical diagnosis at the second study. However, the diagnosis of dyskinesia was reproduced only in two of the four patients. In the other two patients a diagnosis of "stenosis" and "normal" was made at the second study. Cholecystokinin octapeptide (20 ng/kg intravenous bolus) produced inhibition of phasic contractions in all studies, both initially and at three months. We conclude that endoscopic sphincter of Oddi manometry is reproducible when the initial diagnosis is either normal or stenosis. However, the diagnosis of dyskinesia is poorly reproducible, perhaps due to the episodic nature of this manometric disorder or to progression of sphincter of Oddi dysfunction.