Enteric nervous system: intestinal absorption and secretion.
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Humans↗
Biomedical subjects
S Guandalini
Publications and source records attributed to S Guandalini.
A multicentre study on behalf of the European Society of Paediatric Gastroenterology and Nutrition Working Group on Acute Diarrhoea. Early feeding in childhood gastroenteritis.
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Cohort Studies↗
Guidelines prepared by the ESPGAN Working Group on Acute Diarrhoea. Recommendations for feeding in childhood gastroenteritis. European Society of Pediatric Gastroenterology and Nutrition.
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Child↗
Salivary immunoglobulin G assay to diagnose Helicobacter pylori infection in children.
An in-house enzyme-linked immunosorbent assay (ELISA) for measurement of Helicobacter pylori-specific immunoglobulin G (IgG) and IgA in saliva was evaluated by comparison with histopathologic (Giemsa staining) and biochemical (urease quick test) examination of gastric biopsy specimens obtained from 112 children referred for diagnostic gastroscopy. Serum H. pylori IgG was also measured in a subgroup of 50 children by the same ELISA. Salivary H. pylori IgG levels were significantly higher in H. pylori-positive (n = 57) than in H. pylori-negative (n = 55) children (P < 0.001). The sensitivity and specificity of the salivary IgG test were 93 and 82%, respectively; the positive and negative predictive values were 84 and 92%, respectively; and the accuracy was 87.5%. Salivary H. pylori IgA did not distinguish H. pylori-positive from H. pylori-negative children. The performance of serum H. pylori IgG was slightly (3 to 6%) better than that of salivary H. pylori IgG. The salivary IgG test can be considered a useful tool for the screening of H. pylori infection in children.
Adolescent↗
Thyroxine effect on intestinal Cl-/HCO3- exchange in hypo- and hyperthyroid rats.
Changes in transepithelial water and electrolyte transport as causative or contributing factors of the diarrhoea and constipation found associated with changes in thyroid physiology were studied. Albino Wistar rats were pharmacologically made either hypothyroid or hyperthyroid. After sacrifice, the small intestine was mounted in Ussing chambers in order to measure in vitro ion net fluxes under short-circuit conditions. Hypothyroid animals showed an increase in intestinal transit time, Cl- absorption (mainly due to an increment in its mucosal to serosal component) and residual ion flux (which is believed to represent HCO3- secretion) when compared with euthyroid animals. The hyperthyroid animals showed a decrease in Cl- mucosal to serosal transport. Furthermore, a significant correlation was found between serum L-thyroxine (T4) levels and both net Cl- transport (r = -0.74, P < 0.00001) and residual ion flux (r = -0.55, P < 0.005). These results indicate that the effect of T4 is firstly to inhibit Cl-/HCO3- anion exchange thereby influencing transepithelial flux transport and secondly to affect intestinal motility. Such inhibition was not found when T4 was acutely added to rat ileum, suggesting that the effect on electrolyte transport probably requires protein synthesis. In conclusion, the phenomenon observed in vitro could explain the clinical manifestations of constipation and diarrhoea in hypo- and hyper-thyroidism respectively.
Animals↗
Cholera toxin-induced small intestinal secretion has a secretory effect on the colon of the rat.
BACKGROUND/AIMS: Little information is available on the role of colon during small intestinal secretion. The aim of this study was to examine the effects of secretory changes in the small intestine on the colonic transport of electrolytes and water in vivo. METHODS: The jejunum and colon of the rat were perfused in vivo simultaneously but separately, and jejunal secretion was induced by exposing the jejunum to cholera toxin, 8-bromo-cyclic guanosine monophosphate, or hyperosmolarity. RESULTS: Jejunal perfusion with a hyperosmolar mannitol solution (600 mOsm/L) or with 8-bromo-cyclic guanosine monophosphate (0.5 mmol/L) resulted in net secretion of water in the jejunum but did not affect the baseline rate of water transport in the colon. On the contrary, addition of cholera toxin (1 microgram/loop) to the jejunal segment not only induced a significant local secretory change but also resulted in a similar change in the colon, which was not exposed to cholera toxin. The intestine was transected immediately below the jejunum, thus interrupting the anatomical continuity of the enteric nervous system. This procedure eliminated the distant secretory effect of cholera toxin, thus allowing the conclusion that the enteric nervous system is involved in the distant propagation of the local secretion induced by cholera toxin. CONCLUSIONS: Cholera toxin, but not other secretagogues, triggers a secretory response that is not only local but also extends to distal segments via the enteric nervous system.
Animals↗
Calcium-dependent intestinal chloride secretion by Vibrio parahaemolyticus thermostable direct hemolysin in a rabbit model.
BACKGROUND & AIMS: Vibrio parahaemolyticus is a major agent of seafood gastroenteritis that induces intestinal secretion in the rabbit through its thermostable direct hemolysin. The aim of this study was to characterize the enterotoxicity of purified hemolysin in vitro. METHODS: Rabbit ileum was mounted in Ussing chambers, and changes in potential difference and short-circuit current were monitored after addition of hemolysin. Intracellular calcium concentrations in the nontumoral rat crypt-derived cell line IEC-6 were measured using microspectrofluorometry. RESULTS: In Ussing chamber experiments, mucosal toxin addition up to 50 hemolytic units per milliliter induced a proportional increase of the electrical parameters in normal but not Cl(-)-free Ringer's solution. The response to the toxin was not additive to that of calcium ionophore A23187 and was eliminated by preloading the tissue with 1-2-bis(o-aminophenoxy)ethane N,N,N',N'-tetraacetic acid (BAPTA), a calcium buffer. In IEC-6 cells, a 10-fold increase in intracellular calcium level was found after addition of hemolysin. Such an increase was totally quenched by BAPTA. Finally, preincubation with trisialoganglioside GT1b, but not monosialoganglioside GM1, eliminated toxin-induced increases in potential difference and short-circuit current. CONCLUSIONS: These data support the hypothesis that the thermostable direct hemolysin induces intestinal chloride secretion using GT1b as a putative receptor and Ca2+ as a second messenger.
Animals↗
Hansenula anomala killer toxin induces secretion and severe acute injury in the rat intestine.
BACKGROUND & AIMS: The yeast Hansenula anomala has been associated with gastrointestinal symptomatology and damage to the intestinal wall in humans. In vitro and in vivo, H. anomala secretes a toxin, killer toxin, which is lethal to other microorganisms. In view of the very high rate of killer phenotype expression recorded for H. anomala strains in nature, this study aimed to investigate the hypothesis that H. anomala killer toxin plays a role in the pathogenesis of H. anomala-induced enteritis. METHODS: Effects of active and heat-inactivated H. anomala killer toxin on intestinal fluid homeostasis and electrolyte balance were investigated in rat small intestine using a standard intestinal perfusion technique. Sections of the perfused jejunum tracts were examined histologically. RESULTS: H. anomala killer toxin induced a significant secretion of water and electrolytes. No significant change was observed when either heat-inactivated H. anomala killer toxin or control growth medium were tested. Histological analysis showed ischemic degeneration of villi and sloughing of surface epithelium in 50% of active H. anomala killer toxin-perfused jejuna. CONCLUSIONS: This paper presents original observations compatible with the hypothesis that H. anomala killer toxin plays a role in the pathogenesis of H. anomala-induced enteritis.
Animals↗
Etiology and risk factors of severe and protracted diarrhea.
Severe and protracted diarrhea (SPD) is the most severe form of diarrhea in infancy and has also been defined as intractable diarrhea. Its etiology is poorly defined. We have retrospectively evaluated the etiology, the outcome, and the risk factors of 38 children, admitted with protracted diarrhea and need for total parenteral nutrition (TPN) from 1977 to 1993. Children with anatomic abnormalities and/or primary immunodeficiency were excluded. There was an inverse relationship between the number of patients and the age of diarrheal onset (mean age, 2.9 +/- 3.5 months). Etiology of SPD was an enteric infection in 18 cases (eight Salmonella, three Staphylococcus, five rotavirus, one adenovirus, one Cryptosporidium), multiple alimentary intolerance (eight cases), familial microvillous atrophy (two), autoimmune enteropathy (two), celiac disease, lymphangectasia, eosinophilic enteropathy, intestinal pseudoobstruction, and intestinal neurodysplasia (1 case each). Etiology was not detected in three cases. Overall, 12 children died, five are presently being treated, and 21 had full remission. Comparative evaluation of risk factors between children with SPD and a control population of children with diarrhea but without the need for TPN showed that low birth weight, no breast feeding, history of fatal diarrhea in a relative, and early onset of diarrhea had a significantly higher incidence in the former. Social background was similar in the two populations. We conclude that a specific etiology can be identified in the majority of cases of SPD. The etiologic spectrum of SPD is broad, but an enteric infection is the most common cause of SPD. The severity of this condition is related, at least in part, to established risk factors.
Adenovirus Infections, Human↗
Prospective study of lactose absorption during cancer chemotherapy: feasibility of a yogurt-supplemented diet in lactose malabsorbers.
Chemotherapy is a recognized cause of morphological alterations to the proximal intestine. Lactose malabsorption, the functional consequence of a small intestinal enzymatic derangement, has been shown to play an important role in causing gastrointestinal symptoms in subjects receiving chemotherapy. To establish a rational basis for the exclusion of lactose from the diet and to reduce the risk of developing gastrointestinal symptoms, we conducted a study of lactose absorption in 20 children during cancer chemotherapy. Because lactose is an important nutritional sugar, the tolerance of lactose provided by yogurt was examined. Lactose absorption was investigated by a hydrogen breath test (BT) after oral ingestion of milk (250 ml) containing physiological doses of lactose (12 g). The effect of yogurt supplementation was also tested by BT after meals of yogurt (450 g) also containing physiological doses of lactose (12.1 g). In 11 children, lactose malabsorption was detected by BT during the study before any gastrointestinal symptom revealed this status. Of these 11 children, no gastrointestinal discomfort developed in five receiving a lactose-excluded diet. In contrast, in the six children not restricted in lactose intake, gastrointestinal symptoms were observed 4 to 13 weeks after lactose malabsorption was detected by BT. The findings of our study suggested the usefulness of dietary supplementation with yogurt, a lactose-containing food, in children who developed lactose malabsorption. In fact, all lactose-malabsorbent children showed good lactose absorption and tolerance when tested by yogurt BT.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Asymptomatic carriage of intestinal Cryptosporidium in immunocompetent and immunodeficient children: a prospective study.
Little information is available on asymptomatic carriage of Cryptosporidium in immunocompetent and immunodeficient children. We prospectively studied a group of asymptomatic children, 78 immunocompetent and 50 immunodeficient, to document the incidence of asymptomatic carriage of cryptosporidiosis in such a population. We also investigated whether the treatment of children who carried asymptomatic cryptosporidiosis could help in reducing their risk of gastrointestinal symptoms as well as the shedding of infectious oocysts. The occurrence of multiple infections with common intestinal pathogens including Giardia lamblia was also investigated. Asymptomatic cryptosporidiosis was documented in 6.4% of immunocompetent and 22% of immunodeficient children. In a control symptomatic population Cryptosporidium was found in 4.4% of immunocompetent and 4.8% of immunodeficient children. Asymptomatic carriage of Cryptosporidium was documented in 2 human immunodeficiency virus-infected children, one of whom also carried Giardia asymptomatically. Treatment with spiramycin (100 mg/kg daily for 14 days) reduced significantly the duration of the shedding of potentially infectious oocysts. Finally no gastrointestinal symptoms developed in children treated for asymptomatic infection with Cryptosporidium, whereas children who were not treated developed gastrointestinal symptoms.
Adolescent↗
Shigella enterotoxin 1: an enterotoxin of Shigella flexneri 2a active in rabbit small intestine in vivo and in vitro.
Culture filtrates of Shigella flexneri 2a strain M4243 grown in iron-depleted medium, caused significant fluid accumulation in rabbit ileal loops. Also, when tested in Ussing chambers, a greater rise in potential difference and short circuit current was seen with such filtrates compared with the medium control. Analogous filtrates from two M4243 derivatives lacking the 140-MD invasiveness plasmid (either M4243avir or BS103) retained 60-65% of the wild-type enterotoxic activity. Ultrafiltration and gel exclusion size fractionation of M4243 filtrate revealed that the activity was approximately 60 kD. SDS-PAGE performed on this fraction showed 18 bands, 5 of which reacted with human convalescent sera. Genes encoding this enterotoxin, named ShET1 for Shigella enterotoxin 1, were cloned from the S. flexneri 2a chromosome, and two separate open reading frames of 534 and 186 bp were sequenced. These observations suggest that S. flexneri 2a elaborates two distinct enterotoxins: ShET1, encoded by genes located on the chromosome, and ShET2, encoded by a gene on the 140-MD invasiveness plasmid. ShET1, which is composed of two distinct subunits and is elaborated in vivo, where it elicits an immune response, may be important in the pathogenesis of diarrheal illness due to S. flexneri 2a.
Amino Acid Sequence↗
Zonula occludens toxin modulates tight junctions through protein kinase C-dependent actin reorganization, in vitro.
The intracellular signaling involved in the mechanism of action of zonula occludens toxin (ZOT) was studied using several in vitro and ex vivo models. ZOT showed a selective effect among various cell lines tested, suggesting that it may interact with a specific receptor, whose surface expression on various cells differs. When tested in IEC6 cell monolayers, ZOT-containing supernatants induced a redistribution of the F-actin cytoskeleton. Similar results were obtained with rabbit ileal mucosa, where the reorganization of F-actin paralleled the increase in tissue permeability. In endothelial cells, the cytoskeletal rearrangement involved a decrease of the soluble G-actin pool (-27%) and a reciprocal increase in the filamentous F-actin pool (+22%). This actin polymerization was time- and dose-dependent, and was reversible. Pretreatment with a specific protein kinase C inhibitor, CGP41251, completely abolished the ZOT effects on both tissue permeability and actin polymerization. In IEC6 cells ZOT induced a peak increment of the PKC-alpha isoform after 3 min incubation. Taken together, these results suggest that ZOT activates a complex intracellular cascade of events that regulate tight junction permeability, probably mimicking the effect of physiologic modulator(s) of epithelial barrier function.
Actins↗
Effects of deconjugated bile acids on electrolyte and nutrient transport in the rabbit small intestine in vitro.
To obtain new information on the poorly investigated mechanisms of the diarrheogenic effects of bile acids, we investigated the effects of the unconjugated bile acids chenodeoxycholate and ursodeoxycholate on the small intestine transport of electrolytes and nutrients in the rabbit jejunal and ileal mucosa mounted in vitro in Ussing or influx chambers. When added to the ileal mucosa at a concentration of 1 mM, both bile acids induced a secretory shift in ion transport; absorption of Na and Cl was abolished and secretion of bicarbonate was enhanced. No changes in short circuit current or electrolyte transport were observed when the bile acids were added to the jejunal mucosa. The addition of 1 mM chenodeoxycholate to the luminal side of the ileum induced a marked inhibition in the uptake of glucose, phenylalanine, and glutamic acid. A similar inhibition, though of a lesser magnitude, was also induced by both bile acids on jejunal nutrient transport. Further studies on the inhibitory effect of chenodeoxycholate on glucose influx showed that the inhibition was dose-dependent; at 1 mM it was maximal and resulted in the complete abolition of the active component, with only the diffusional pathway still operative. We conclude that unconjugated bile acids act as secretagogues in the ileum and significantly blunt the active transport of nutrients in the small intestine. Both effects may well play a role in the diarrheogenic action of these bile acids.
Animal Nutritional Physiological Phenomena↗
Enteroaggregative Escherichia coli heat-stable enterotoxin 1 represents another subfamily of E. coli heat-stable toxin.
Enteroaggregative Escherichia coli (EAggEC) are associated with persistent diarrhea in young children. Some of these organisms produce a low-molecular-weight, heat-stable, plasmid-encoded enterotoxin that has been named EAggEC heat-stable enterotoxin 1 (EAST1). We have cloned a 4.4-kb DNA fragment from the virulence plasmid of prototype EAggEC strain 17-2, which expresses enterotoxic activity as measured by electrogenic response in Ussing chambers mounted with rabbit ileal tissue. DNA-sequence analysis of this fragment identified an open reading frame (ORF) encoding a cysteine-rich polypeptide of 38 amino acids (M(r), 4100). Insertional and deletional mutations in this ORF resulted in loss of enterotoxic activity. The ORF was cloned into a T7 expression vector, and postinduction culture filtrates exhibited enterotoxic activity and increased ileal tissue cGMP levels. A synthetic peptide consisting of predicted amino acid residues 8-29 also showed enterotoxic activity. These data indicate that this ORF, named astA (EAggEC heat-stable enterotoxin), represents the EAST1 structural gene. EAST1 shows significant homology with the enterotoxic domain of heat-stable enterotoxin a (STa) of enterotoxigenic E. coli and with guanylin, a mammalian analog of STa. Unlike STa, which requires six cysteines and three disulfide linkages for full biological activity, both EAST1 and guanylin contain four cysteine residues. Based on the cGMP data and the sequence homology to STa and guanylin, it is predicted that EAST1 stimulates the particulate form of guanylate cyclase through the same receptor-binding region as STa and guanylin.
Amino Acid Sequence↗
Reference values of the steatocrit and its modifications in diarrheal diseases.
Conflicting results have been reported on the use of the steatocrit to measure fecal fat excretion. Aiming to assess the reliability of this method and its usefulness in the diagnosis of intestinal enteropathies, we measured the steatocrit in 747 healthy children and 442 children with diarrhea grouped according to diagnosis. The steatocrit was found to correlate strictly (r = 0.93) with the chemical measurement of fecal fat. Reference values and ranges were established. The maximal steatocrit was observed in neonates; afterwards, it progressively decreased to an undetectable level in children older than 2 years of age. A steatocrit abnormally high for age was found in 20% of patients with acute diarrhea and in 53% of those with chronic diarrhea. All celiac patients with a gluten-containing diet showed a marked increase of steatocrit. We conclude that the steatocrit is a reliable and easy-to-perform test, which quickly provides valuable information in the diagnostic workup of the child with diarrhea.
Adolescent↗
Transient gluten hypersensitivity.
We report a case of transient gluten hypersensitivity, demonstrated by jejunal histology at diagnosis, normalization after gluten-free diet, and acute clinical and histological relapse after a challenge with gluten powder at the age of 1 year, resembling that observed in cow's milk protein intolerance. Subsequent provocation tests did not show any alteration. Cases of supposed transient gluten hypersensitivity are rarely reported; our patient is characterized by the acute reaction to gluten challenge associated with a damaged histological picture and depressed levels of complement.
Duodenum↗
Impaired intestinal function in symptomatic HIV infection.
A longitudinal (10-22 month) evaluation of intestinal symptoms and function was performed in five children with symptomatic human immunodeficiency virus (HIV) infection. All received cotrimoxazole, ketoconazole, and immunoglobulins. A search for enteric pathogens and intestinal function tests were repeatedly performed in all patients. Mild episodes of diarrhea were observed in two children. One had cow's milk protein intolerance. Giardia lamblia was found in an asymptomatic carrier. Evidence for impaired intestinal function was found in all patients. These consisted of positive D-xylose and iron oral loads, increased steatorrhea, increased fecal excretion of alpha 1-antitrypsin, abnormal intestinal permeability, and increased food antibody levels. Our results suggest that severe diarrhea may be uncommon in children with HIV infection receiving antimicrobial prophylaxis, but that the intestinal function is frequently, and often markedly, impaired.
Antibodies↗