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BACKGROUND: Obesity is associated with low-grade inflammation contributing to insulin-resistance. Gut barrier alterations, described in animal models of obesity, probably favour inflammation. This has not been hitherto described in obese humans. AIM: To evaluate gut permeability in asymptomatic obese and its association with plasma (C-reactive protein (CRP), arachidonate/eicosapentaenoate ratio) and faecal (calprotectin and leptin) markers of inflammation and microbiota alterations. METHODS: A total of 13 obese (age: 33.9 ± 11.5 years; BMI: 35.9 ± 5.0 kg/m²) and 11 control subjects (age: 30.3 ± 8.1 years; BMI: 23.5 ± 2.4 kg/m²) were recruited. Gut permeability was assessed by the lactulose-mannitol-sucralose test, plasma fatty acids by gas chromatography, faecal calprotectin and leptin by Elisa and faecal microbiota by G+C profiling. RESULTS: C-reactive protein was increased in the obese subjects (P = 0.01), but neither the plasma arachidonate/eicosapentaenoate ratio, the faecal levels of calprotectin and leptin, nor the gut permeability were altered. The faecal microbiota was altered in the obese (P = 0.0002), with predominance of bacterial populations having a lower G+C content and decreased concentrations of high G+C populations. CONCLUSIONS: Asymptomatic obese individuals with systemic low-grade inflammation do not have evidence of colonic inflammation or gut barrier alteration; however, the biodiversity of their intestinal microbiota is affected.

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OBJECTIVES: Amoxicillin is a beta-lactam antibiotic largely used in childhood. However only few studies described its impact on composition of children gut microbiota, in particular on Bifidobacterium populations considered as beneficial microorganisms. In this study, the impact on faecal Bifidobacterium species of a seven-day amoxicillin treatment was quantitatively and qualitatively assessed in infants during an episode of acute respiratory infection. METHODS: Faecal samples from 31 infants were obtained on day 0 (just before amoxicillin therapy) and on day 7 (the end of therapy). Total DNA was extracted and bifidobacteria were quantified using real-time PCR. Predominant Bifidobacterium species were then identified using specific PCR-TTGE. RESULTS: Bifidobacteria concentrations were not significantly altered by amoxicillin compared to the healthy group. However, amoxicillin treatment induced a complete disappearance of Bifidobacterium adolescentis species (occurrence rate of 0% versus 36.4% in healthy group, P < 0.001), a significant decrease in the occurrence rate of Bifidobacterium bifidum (23% versus 54.5% in healthy group, P < 0.05), but did not affect Bifidobacterium longum (93.5% versus 100% in healthy group) and Bifidobacterium pseudocatenulatum/B. catenulatum (about 55% in both groups). The number of Bifidobacterium species per microbiota significantly decreased from 2.5 +/- 1 for healthy group to 1.8 +/- 0.9 for treated infants (P < 0.05). CONCLUSIONS: This study showed that a 7 day amoxicillin treatment did not alter the counts of Bifidobacterium. However amoxicillin can have an impact by changing the microbiota at the species level and decreased the diversity of this population.

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La función de barrera intestinal se encuentra alterada en los pacientes quemados; supone una probable fuente de traslocación bacteriana que puede tener como resultado un fallo orgánico múltiple en estos pacientes. No sabemos cuánto tarda esta función en recuperarse hasta valores normales y no conocemos cómo se encuentra la función de barrera gástrica en los pacientes quemados. El propósito de este estudio es intentar responder a estas cuestiones, observando el ritmo de normalización de la función de barrera intestinal y lo que ocurre con la permeabilidad gástrica en este tipo de pacientes. Estudiamos un total de 15 pacientes (10 varones y 5 mujeres), grandes quemados, con un promedio de superficie corporal quemada (SCQ) de un 18% (+/-7,4), con quemaduras de 2° y 3° grados de Converse Smith, ingresados hasta 24 horas después de producirse la quemadura, a los que se les realizó test de permeabilidad gastrointestinal a las 24 horas y los días 3, 7,14 y 21 postquemadura; elaboramos curvas de permeabilidad gástrica e intestinal y, posteriormente, se compararon con las permeabilidades obtenidas de 18 individuos sanos control. .Observamos que la excreción de sacarosa al ingreso fue de 94,6 (44,7-198,3 mg.), 5 veces mayor que la de los individuos sanos; aunque hubo disminución progresiva de estos niveles de excreción , a las 3 semanas todavía no se habían alcanzado los valores de los individuos sanos. En cuanto a la relación de lactulosa/manitol , en los pacientes quemados fue de 0,080 (0,042-0,153 %), 4,4 veces mayor que la de los individuos sanos; sólo se alcanzaron los niveles de éstos 2 semanas después de la quemadura. No se observó correlación entre la SCQ y los valores de sacarosa y lactulosa/manitol. Existe por tanto una fuerte alteración de la permeabilidad gástrica e intestinal en pacientes quemados, que comienza a normalizarse alrededor de la segunda semana postquemadura para la permeabilidad intestinal, mientras que la permeabilidad gástrica tarda más en normalizarse, no alcanzando los valores normales durante las 3 semanas que duró este estudio (AU)

Gut barrier function is impaired in burn patients, leading to increased odds of bacterial penetration and resulting in multiple organic failure. It is unknown how long does it take to the normalization of the gut barrier, nor the gastric barrier. The purpose of our study is trying to answer those questions, analyzing the rate of gastric permeability and gut barrier normalization in this kind of patients We studied 15 burn patients, 10 males and 5 females, with medium burn total body surface of 18%(+/- 7,4) , with 2nd and 3rd degree burn injuries according to the Converse Smith classification, hospitalized within the first 24 hours of injury. Gastric and intestinal permeability were measured in 24h, and days 3rd, 7th, 14th and 21st after injury and compared with 18 normal patients as controls. Sacarose excretion on admission was 94,6 (44,7-198,3 mg), 5 times higher than controls; these levels decreased within the 3 weeks of the study, but never reached the levels of the controls subjects. In contrast, the rate lactulose/manitol, 0,080 (0,042-0,153%) was 4 times higher than controls on day 1st, but reached normal levels after 2 weeks. The levels of sacarose and lactulose/manitol were not related to burn total body surface. There is a strong correlation between gastric and gut permeability in burn patients. The intestinal permeability takes about 2 weeks to begin to normalize, and the gastric permeability improves but did not normalize during the 3 week duration of this study (AU)

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Fermented foods have been used since prehistoric times. Their number, variety and geographic origin are considerable, and different substrates and agents including bacteria, yeasts and moulds have been used in their preparation. In the last few decades the scientific approach to the study of the participating microorganisms and the resulting products have provided a better understanding of their biological importance. Among the many health-related properties of fermented foods, effects on blood pressure have been described after casein hydrolysis by lactic acid bacteria. Peptides with antimicrobial activity, mainly against Gram-negative bacteria, and derived from casein have also been identified. This could explain, at least in part, the antidiarrheal effects of fermented products including those on traveler's diarrhea and against colonization by Helicobacter pylori. One of the best known advantages of fermented milk products is their capacity to improve lactose tolerance in hypolactasic subjects. With the growing prevalence of allergies and inflammatory bowel diseases, considerable interest has been focused on the effects of lactic acid bacteria in these conditions; there is evidence that these agents are associated with improvements in allergy; no such evidence exists for Crohn's disease or ulcerative colitis. A cholesterol-lowering capacity has also been described for some microorganisms. Not all the fermenting microorganisms have probiotic capacities as the latter are strain-specific.

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Helicobacter pylori is a highly prevalent pathogen considered as an aetiological factor for gastroduodenal ulcers, and a risk factor for gastric adenocarcinoma and lymphoma in humans. Most subjects colonized by this micro-organism are asymptomatic and remain untreated. In symptomatic patients, the antibiotic treatment has a high cost and is not 100% effective because of resistance to antibiotics and to moderate patient compliance. This review discusses the role of probiotics as alternative solutions to assist in the control of H. pylori colonization in at-risk populations. The evidence that some strains of Lactobacillus and Bifidobacterium are able to inhibit H. pylori growth through the release of bacteriocins or organic acids, and may also decrease its adhesion to epithelial cells, is reviewed. In addition, probiotics have a possible role in the stabilization of the gastric barrier function and the decrease of mucosal inflammation. Other aspects that are considered are the contribution of probiotics to the healing of the gastric mucosa linked to their antioxidant and anti-inflammatory properties. Clinical trials in colonized adults and children are reviewed, and suggest that probiotics do not eradicate H. pylori but maintain lower levels of this pathogen in the stomach; in combination with antibiotics, probiotics may increase eradication rate and/or decrease adverse effects. Papers suggesting similar effects on H. pylori by foodstuffs such as berry juice and some milk proteins are quoted. Regular intake of these and other dietary products might constitute a low-cost, large-scale alternative solution applicable for populations at-risk for H. pylori colonization.

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Prebiotics increase intestinal levels of health-promoting bacteria implicated in decreasing pathogen colonization, stimulating immune functions and stabilizing gut barrier functions, parameters which are altered in burn patients. We propose that regular intake of a prebiotic, oligofructose (OF), might help to improve the altered gastrointestinal (GI) permeability observed in burn patients. A randomized, double-blind, controlled clinical trial was carried out in 41 burn patients (mean burn surface area=17.1+/-8.2%) who ingested daily 6 g of oligofructose (OF group) or sucrose as placebo (Control group) during 15 days. Gastrointestinal permeability to sucrose and lactulose/mannitol (L/M) was evaluated on days 1 (before treatment) 3, 7, 14 and 21. A permeability test was also performed in 18 healthy subjects as controls. Thirty-one patients completed the protocol (dropout rate=24.4%). Healthy subjects had a basal sucrose excretion of 21.3 mg (14.0-32.5 mg) and a basal L/M ratio of 0.017% (0.009-0.022%). Sucrose excretion increased 5-fold and L/M ratio 4.4-fold in burn patients on day 1 and these high levels of marker excretion decreased significantly throughout the study (p=0.016 and 0.000001, respectively). No differences between the OF and Control groups were observed for sucrose excretion or L/M ratio. In conclusion, the normalization of gastrointestinal permeability is not accelerated by prebiotic intake.

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BACKGROUND: Smoking is a risk factor for gastroduodenal ulcer and gastric adenocarcinoma. However, the pathophysiological mechanisms induced by acute cigarette smoking in the human gastric mucosa are poorly understood. AIM: To evaluate the effect of acute cigarette smoking, alone or with alcohol, on the gastric permeability to sucrose, a specific marker of mucosal damage in the stomach. SUBJECTS AND METHODS: Twenty healthy volunteers (8 smokers/12 non-smokers) were studied. Each fasted subject ingested 500 ml of a 20% sucrose solution and the amount of sucrose excreted in a 5-hour urine collection was measured by gas chromatography Four sucrose permeability tests were carried out: 1. basal, 2. while smoking 5 cigarettes, 3. after drinking 50 ml of a 40 degrees alcoholic beverage, 4. a combination of 2+3. RESULTS: Sucrose excretion increased after alcohol ingestion (40.5 +/- 6.0 mg vs 143.1 +/- 28.9 mg, p = 0.002), but was not modified by acute cigarette smoking (34.4 +/- 5.9 mg). When alcohol and cigarettes were simultaneously consumed, the increase in alcohol-induced sucrose excretion was significantly reduced (73.1 +/- 16.6 mg, p = 0.03). Basal sucrose excretion was similar in smokers and non-smokers. However, in acute cigarette smoking, a decrease in sucrose excretion was observed in smokers (p = 0.02) but not in non-smokers. CONCLUSIONS: These results indicate that acute cigarette smoking may tighten the gastric mucosa in habitual smokers and this is associated with a smaller increase of gastric permeability induced by alcohol.

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AIMS: Gluten ingestion in coeliac disease is associated with alterations of the intestinal mucosa, especially the expansion of the lamina propria. Antiendomysium and antireticulin antibodies may result from interactions between gliadin and extracellular matrix components. By behaving as autoantigens, connective tissue proteins could initiate mucosal damage. This study evaluates changes in the distribution of laminin, type IV collagen, and fibronectin in the mucosa of patients with coeliac disease in an attempt to explain the alterations of mucosal morphology. METHODS: Intestinal biopsies were obtained from patients with coeliac disease on admission and while on a gluten free diet. The distribution of type IV collagen, laminin, fibronectin, and alpha-smooth muscle actin was evaluated by immunofluorescence and by immunogold labelling and electron microscopy. RESULTS: In patients with coeliac disease, the intensity of type IV collagen, laminin, and fibronectin immunofluorescent staining was decreased and less well defined than in controls, with frequent breaches in the basement membrane; fibronectin staining was weak in the distal third of the elongated crypts and absent under the flat surface. The distribution of smooth muscle fibre in the distal lamina propria of flat mucosae was altered. The distribution of these proteins was normal as assessed by immunoelectron microscopy. CONCLUSIONS: The intensity of staining of some components of the basement membrane is decreased in coeliac disease and the distribution of smooth muscle fibres is altered. These changes may result from interactions between gliadin and components of the extracellular matrix and may play a role in the genesis of mucosal lesions and in the damage to the epithelium.

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The differentiation, architecture and function of the mucosa of the digestive tract is the result of close interactions between the epithelial cells and their underlying connective tissue. This interaction not only plays a role in the normal morphological organization of the intestinal mucosa but also in the organization and maturation of the enterocytes, the development of some of their enzymatic activities, the transport of nutrients and the restitution of the epithelium following denudation of the surface of villi due to loss of enterocytes. It is thought that disturbances of the cells of the connective tissue, especially of the myofibroblasts as well as of some of the above mentioned mechanisms, participate in the pathogenesis of some gastrointestinal diseases, celiac disease among them. This review summarizes some of the knowledge in this area.

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Determination of plasma and tissue cytokine levels in inflammatory bowel disease have frequently resulted in conflicting data. In the present study we determined in patients with ulcerative colitis (UC), the levels of the proinflammatory cytokines interleukin (IL)-1beta, IL-6, interferon (IFN)-gamma, and tumor-necrosis factor (TNF)-alpha liberated by peripheral blood mononuclear cells (PBMC) and lamina propria mononuclear cells (LPMC) after 48-hr culture with pokeweed mitogen (PWM). IL-1beta, IL-6, IFN-gamma and TNF-alpha in the supernatant were detected by ELISA. Results show low basal levels of IL-1beta secretion by PBMC and LPMC, and a considerable increase after mitogen stimulation. Basal IL-6 production by PBMC was higher in UC patients than in controls [2029 pg/ml, CI95(-165 to 4223) vs 572 pg/ml (-383 to 1527) respectively, P = 0.05] and also after PWM activation [14,995 pg/ml (7759-22,230) vs 6598 pg/ml (3240-9956), respectively, P = 0.05]. In LPMC, no differences in IL-6 secretion were observed. TNF-alpha in activated PBMC of patients with UC was not significantly increased in relation to control (P = 0.09). No constitutive secretion of IFN-gamma was observed in mononuclear cells. IFN-gamma levels secreted by activated LPMC were lower in patients with UC than in controls [1571 pg/ml (-108 to 3251) vs 7953 pg/ml (3851-12,055), respectively, P = 0.03]. These results suggest that IL-6, IL-1beta, and TNF-alpha participate as mediators in the inflammatory phenomena observed in UC. Further studies are necessary to evaluate the role of IFN-gamma in this condition.

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BACKGROUND: Cytokines are involved in the pathogenesis of inflammatory bowel diseases such as ulcerative colitis and Crohn disease. AIM: To measure cytokine release by mononuclear cells of patients with ulcerative colitis. PATIENTS AND METHODS: Twelve patients subjected to a diagnostic colonoscopy were studied. Six had an ulcerative colitis and six did not have inflammatory changes in the colonic mucosa and were considered as control. Mononuclear cells were isolated from biopsies of colonic mucosa and from peripheral blood cultivated during 48 hours with pokeweed mitogen, and Interleukin 6 and interferon-gamma were measured in their supernatants. RESULTS: In patients with ulcerative colitis, interleukin 6 secretion by peripheral blood mononuclear cells was higher than in control subjects in the basal period (2212 +/- 424 and 443 +/- 174 pg/ml respectively p = 0.03) and after stimulation with pokeweed mitogen (16,328 +/- 1275 and 5462 +/- 322 pg/ml respectively p = 0.03). No differences in interleukin 6 secretion by colonic mucosa mononuclear cells were observed. Unstimulated cells did not liberate interferon-gamma. The secretion of this lymphokine by stimulated colonic mucosa cells was lower in patients with ulcerative colitis than in controls (1571 +/- 216 and 7953 +/- 389 pg/ml respectively p = 0.03). CONCLUSIONS: Local and systemic changes in interleukin 6 and interferon-gamma secretion occur in patients with ulcerative colitis. These changes could be related to the development of the disease.

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The cytoprotective and anti-inflammatory effects of boldine in an experimental model of acute colitis are reported. The administration of boldine to animals with colitis induced by the intrarectal administration of acetic acid, was found to protect against colonic damage as expressed by major reductions in the extent of cell death, tissue disorganization, and edema. Boldine also reduced the colonic neutrophil infiltration, as measured by the myeloperoxidase activity, but it did not significantly affect tissue lipoperoxides. Boldine was found to preserve the colonic fluid transport, a function otherwise markedly affected in the tissue of acid-treated animals. Results presented here provide experimental evidence supporting new cytoprotective and anti-inflammatory properties of boldine.

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BACKGROUND: Increased permeability to sucrose has been recently shown to be a good marker of gastric mucosal damage in adults. METHODS: This test was evaluated in 40 children consulting for recurrent abdominal pain and the results were correlated with endoscopic and histologic findings and with the presence of H. pylori. RESULTS: The gastric mucosa was considered endoscopically normal in 31 children; 3 had duodenitis and 6 had mild gastritis. Abnormal endoscopic findings were associated with increased urinary sucrose excretion (MANOVA F = 7.30; p = 0.002). In the 6 children with mild gastritis, mean sucrose excretion was twice that of controls (0.060 +/- 0.024 vs. 0.029 +/- 0.018, respectively; p = 0.019) and significantly higher than the group with duodenitis (0.037 +/- 0.013; p = 0.038). The specificity and sensitivity of sucrose permeability test for detection of gastric damage were 90.3% and 83.3%, respectively. H. pylori was detected in 62.5% of children including all patients with mild gastritis, in 2 out of 3 with duodenitis and 17 out of 31 endoscopically normal controls. No differences in sucrose excretion were observed in relation with the presence of H. pylori or histological findings in the control group. CONCLUSIONS: Urinary sucrose excretion is a good marker of mucosal gastric damage in children and may be used as a screening test in large groups of populations.

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To test the hypothesis that the increased health risk of children selected by a previously calculated and validated predictive model is associated with some maternal psychological characteristics, the universe of 107 mothers of children selected by this model was evaluated by means of Goldberg's General Health Questionnaire (GHQ-30), Raven (Ra) and Rorschach (Ro) tests; 37.4% were cases according to GHQ-30, 80.9% were < 50th percentile in Ra and 85% exhibited deviant responses in Ro tests. Children whose mother's IQ was < 50th percentile suffered more episodes of total morbidity (Tm) and of diarrhoea (p = 0.0364). Children whose mothers were normal in Ro had less Tm (p = 0.0364) and fewer respiratory symptoms (p = 0.0300) and tended to have less diarrhoea (p = 0.0690). In poor urban families in Santiago psychological maternal characteristics are associated with an increased health risk for the infants. Supportive programmes should consider both biological characteristics of the infants and maternal psychological needs.

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A previously calculated predictive model for health risk selects infants who suffer 4-5 times more morbidity than their unselected peers. Preliminary results suggested that this risk is related to maternal neurotic symptomatology. To evaluate this hypothesis, 52 consecutive mothers whose infants had a positive predictive score (Group 1) and 52 in whom this was negative (Group 2) were evaluated by means of Goldberg's General Health Questionnaire (GHQ-30). A total of 41.9% and 20.5% of the mothers in Groups 1 and 2, respectively, scored above 11 points in GHQ-30, established as the cut off point. It is concluded that among poor urban families in Santiago mothers of infants with high risk of persistent diarrhoea have increased frequency of detectable neurotic symptoms. New programs aimed at this type of infant should include psychological support for their mothers.

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A predictive model which identifies infants who suffer 4 to 5 times more morbidity than their unselected peers was calculated in previous studies, in population of the low socio-economic stratum (SES) (Rev Med Chile 1992; 120: 342-8): Some families of the middle SES also seek care at the Primary Health Care System. Therefore, since our aim is to propose an instrument to be used at this level, the predictive model was applied in families of this stratum. Children identified by means of the model suffered as many episodes of diarrhea but not of other illnesses, as their peers of the low SES (4.8 vs 4.3 respectively). Families in whom the instrument was positive were fewer in the middle SES (6.8 vs 15.7%). Because during the study a campaign to prevent cholera was carried out in Santiago, and this may modify the predictor's performance, at the end of the follow up the model was validated again in families of the low-SES; results confirmed that children with a positive predictor suffered more diarrhea than those of the non-selected population (6.5 vs 3.4 episodes/children/year).

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Two groups of infants (intervention group n = 66, and control group n = 45) at risk of persistent diarrhoea (PD) as identified by a predictive model were followed for 12 months. Families were visited at home weekly; mothers in the intervention group received information about prevention and treatment of diarrhoea and were encouraged to seek help in the field station when their children became ill. These children suffered fewer days with any illness, diarrhoea, or respiratory episodes (p < 0.00001 each). Also, in this group, the incidence of PD decreased to the levels of nonselected population only in children whose mothers consulted for the episode of diarrhoea (2.8%). Results show that the intervention decreased the time children suffered diarrhoea and also respiratory and other illnesses. This suggests that the predictive model identified children with high risk but is not disease-specific. Risk appears to be related to maternal behaviours. The model may be useful in the community for detecting groups vulnerable to common paediatric illnesses, including diarrhoeal disease.

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