This study was undertaken to determine the effect of inflammatory bowel disease (IBD), in general, and one of its manifestations, growth retardation, in particular, on the self-image of adolescents. The conceptualization of adolescent self-image as described by D. Offer (1981) was the basis for the study's framework. The psychological, social, sexual, familial and coping selves, further classified into 11 separate content areas, comprised the adolescent self-image. A descriptive-comparative design was used to describe the self-image of adolescents with IBD and to compare the similarities and differences in self-image among the IBD adolescents with and without growth retardation and their healthy peers. A convenience sampling method was used to obtain 24 IBD subjects between the ages of 12 and 20, eleven of whom had growth retardation. A normative sample of adolescents (N = 1385) was used by permission of D. Offer for purposes of comparison with the IBD subjects. Data were gathered using the Offer Self-image Questionnaire for adolescents. The adolescents with IBD did not differ remarkably from the norm in their perceptions of self although a tendency among the females to have concerns about their body image and sexual maturation was demonstrated. The IBD subgroup without growth retardation reported self-image perceptions that were superior to the norm and the growth retarded subgroup in almost every category. The IBD subgroup with growth retardation reported a disturbed self-image in a number of areas. The males revealed disturbances primarily in body image and secondarily in emotional harmony, and adaptability to stress in the immediate environment, family relations, and sexual maturation. The females revealed self-image disturbances in sexual maturation and body image. The findings of the study suggest that growth retardation in the IBD adolescent may have a negative effect on self-image. The findings may demonstrate a more notable and broader effect of growth retardation on self-image in the males with IBD than in the females. / Applied Science, Faculty of / Nursing, School of / Graduate

PDase II activity was determined using a synthetic substrate, the 2,4-dinitrophenyl ester of thymidine 3'-phosphate. The enzyme activity was estimated in fractions obtained by differential centrifugation of homogenates of epithelial cells fromt.the small intestinal mucosa of guinea pigs and rats. In guinea pig preparations PDase II occurred with highest specific activity in those fractions rich in succinate dehydrogenase and acid phosphatase. A lysosomal location for the guinea pig enzyme was indicated by its structure-linked latency and by its association with particles which underwent a characteristic decrease in equilibrium density when Triton WR-1339 was injected into the animals. With rat preparations a much greater proportion of the PDase II activity was found in the soluble fraction after uult-ra;c;entrifugation. The rat enzyme exhibited a lower degree of latency and administration of Triton WR-1339 had no effect. The rat enzyme activity in these crude preparations further differed from that of the guinea pig in other respects; it was more labile at 60°C, exhibited a slightly lower pH optimum, had a higher molecular weight as determined by gel filtration chromatography and displayed a much smaller tendency to aggregate under Llow salt conditions. Both enzymes were purified by chromatography on DEAE-cellulose, CM-cellulose and agarose, the extensive purification (550 fold) of the rat enzyme being largely due to its behaviour oh the latter material where it was found to bind tenaciously in low ionic strength solutions. On the other hand, only a fifteen-fold purification of the guinea pig enzyme was obtained because of its tendency tofform insoluble aggregatesdduring the chromatographic steps. In the main, the properties of the partially purified enzymes were quite similar. Both displayed pH optima between pH 6 and 7, were inhibited in solutions of high ionic strength, were unaffected' by divalent cations or EDTA, were similarly inactivated by heating at a temperature of 60°G displayed discontinuous Arrhenius plots _5 and exhibited Km values of the order 2-5x10 M for dTpDNP. In most casestfche differences between the enzymes were just differences of degree and could probably be accounted for byethe different extents to which the enzymes were purified. A more extensive characterization of the highly purified rat PDase was carried out. The fall-off in PDase II reaction rate observed at high enzyme levels with dTpDNP as substrate was found to be due to competitive inhibition of the enzyme by dTp, a reaction product which showed a of 2x10 M. The isoelectric point of PDase II was estimated by electrofocusing but since multiple peaks of activity were found at pH 3.4, 4.2-4.5, and pH 7.2 a conclusive result was not obtained. Polyacrylamide gel electrophoresis of purified rat PDase II indicated that the pattern obtained was, in part, dependent on whether the preparation was fresh or not; freshly purified PDase II contained up to 10 bands in gels stained for protein whereas only 1-2 bands were obtained when the preparations were "aged". A molecular weight of 150000-170000 for the enzyme was estimated in experiments performed by gel-filtration chromatography on dextran and agarose gels. Investigation of the interaction with, and hydrolysis by, rat PDase II of a number of possible phosphodiester substrates indicated that'-, the enzyme required a nucleoside 3'-phosphoryl residue for the initiation of hydrolysis which then proceeded in a 5'+3' direction. Finally, the effect of some enzyme inhibitors was investigated. PDase II activity was inhibited in the presence; of NEM, PCMB, PCMPS and iodoacetic acid. It was further found that the inactivation by iodoacetic acid could be prevented by the presence of a PDase substrate or, better still, by dTp. This is good evidence that iodoacetate alkylates an essential residue at the active center of PDase II and is the first time that such an effect has been shown for a PDase. / Medicine, Faculty of / Biochemistry and Molecular Biology, Department of / Graduate

Orientador: Pedro Luiz Rosalen / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba / Made available in DSpace on 2018-07-19T15:53:46Z (GMT). No. of bitstreams: 1 DelFiol_FernandodeSa_M.pdf: 1505001 bytes, checksum: 265a879fb9127a4758242b8ad95fd302 (MD5) Previous issue date: 1994 / Resumo: A proposta do presente estudo foi avaliar a interferência da alimentação na absorção gastrointestinal de flúor ingerido através de dentifrício fluoretado. Dezoito voluntários adultos jovens foram submetidos a três situações de conteúdo estomacal, jejum, café da manhã e almoço e à ingestão de um dentifrício em 3 concentrações; placebo, 550 e 1100 ppmF, ou seja, em ocasiões diferentes ingeriram um dentifrício em cada situação de conteúdo gástrico. Foram feitas coletas de urina 24 horas anteriores e posteriores ao experimento e a partir da ingestão do dentifrício, amostras de saliva foram coletadas nos tempos (hora) 0; 0,25; 0,5; 0,75; 1,0; 2,0; 3,0; 8,0 e 24. Através da área de concentração salivar e da quantidade de flúor excretada em cada tratamento e pôde-se notar uma queda na absorção em torno de 19% quando da ingestão de flúor após o café da manhã e de aproximadamente 33% quando da ingestão de flúor após uma refeição tipo almoço / Abstract: The aim of the present study was to determine the influence of feed in the gastrointestinal absorption of fluoride ingested as fluoride dentifrices. Eighteen young volunteers were submited to three situations of stomachal contents; fasting stomach, breakfast and lunch and then to ingest some fluoride dentifrice in three different concentrations; placebo, 550 and 1100 ppmF, i.e., in different occasions they ingested one dentifrice in a situation of stomachal content. Urine was colected 24h before and after the experiment and as soon they ingested the dentifrice, saliva samples were colected in time (hour) 0; 0,25; 0,5; 0,75; 1,0; 2,0; 3,0, 8,0 and 24,0. Data from salivary fluoride concentration (ASC) and F urinary output was determined. In the present study it was found that breakfast and lunch consumed prior to ingestion of fluoride reduces fluoride absorption by 19% and 33% respectiviJy, compared to ingestion on a fasting stomach / Mestrado / Farmacologia / Mestre em Odontologia

Tesis entregada a la Universidad de Chile en cumplimiento parcial de los requisitos para optar al grado de Doctor en Ciencias con mención en Microbiología / La mayor concentración y diversidad de microorganismos asociados a la microbiota humana reside en el intestino, estableciendo una relación comensal o mutualista con el hospedero, la cual puede verse interrumpida cuando la estructura y composición microbiana es alterada (disbiosis). La disbiosis puede estar asociada a cambios en la dieta, el uso de antibióticos y en una serie de enfermedades, entre ellas las enfermedades inflamatorias intestinales (EII) como Colitis Ulcerosa (CU) y Enfermedad de Crohn (EC). Si bien la mayor parte de los estudios sobre microbiota intestinal se han realizado a partir muestras de heces debido a su fácil obtención, la microbiota adherente del colon es la más representativa de la comunidad microbiológica que co-evoluciona con el hospedero en el transcurso de la enfermedad, pues ésta puede interactuar de forma más directa con el sistema inmunitario. Considerando los antecedentes expuestos el objetivo de esta tesis es la caracterización de la microbiota adherente de individuos con EII mediante análisis de secuenciación masiva y generación de librerías de rDNA16S, a partir de muestras de biopsias de individuos chilenos y españoles (n=66) diagnosticados con EC, CU y controles (CTL). Nuestros resultados mostraron diferencias significativas entre la abundancia relativa de las phyla Proteobactería y Firmicutes entre individuos con EII y CTL, sin embargo no observamos diferencias significativas entre la microbiota de individuos con CU y EC. Por otro lado, a diferencia de los estudios realizados con muestras de heces, donde los individuos con EII fueron clasificados en grupos únicos y definidos (EC, CU o CTL), en nuestro estudio los individuos con EII se clasificaron en 5 grupos distintos según su composición microbiana. Los grupo denominados EII-1, EII-3, EII-2 y EII-5 albergaron únicamente individuos con EC y CU, presentando un enriquecimiento de las phyla Bacteroidetes (34.5%), Proteobacteria (75.4%), y de las Unidades Filogenéticas Operacionales (OPUs) afiliadas a las bacterias Ruminococcus gnavus (9.75%); Cupriavidus necator/Ralstonia pickettii (6.60%); Brevundimonas diminuta/Brevundimonas vancanneytii (5.87%) y Klebsiella oxytoca (32.16%). El grupo EII-4 contuvo individuos con EII y CTL mostrando un enriquecimiento del phylum Firmicutes (59.85%) y OPUs afiliados a Faecalibacterium prausnitzii (14.67%), (bacteria características de individuos sanos). Sumado a los anterior aquellos individuos pertenecientes a los grupos EII-3, EII-2 y EII-5 presentaron abundancias que abarcaron entre el 12.74 al 55.60% en OPUs afiliados a bacterias anaeróbicas facultativas y abundancias del 4.25% al 9.68% en OPUs afiliados a bacterias aeróbias estrictas. Por el contrario, los grupos EII-4 y EII-1 abarcaron abundancias del 41.21% al 45.3% en OPUs afiliados a bacterias anaerobias obligadas y abundancias cercanas al 1.5% en OPUs afiliados a bacterias aerobias estrictas. Además, los análisis de correlación mostraron asociaciones negativas entre los OPUs anaerobios facultativos o aerobios, (indicadores de individuos con EII pertenecientes a los grupos EII-1, EII-2, EII-3, EII-5) con aquellos OPUs anaerobios (indicadoras de EII-4). Este tipo de correlación da cuenta de relaciones de competencia (exclusión) entre estas bacterias, dadas posiblemente por las condiciones ambientales del intestino, es decir un incremento en los niveles de oxígeno durante el proceso de inflamación. Estos resultados concuerdan con lo sugerido en la “hipótesis del oxígeno”, donde se plantea que en condiciones de inflamación crónica las paredes intestinales de individuos con EII conducen a una mayor liberación de hemoglobina (que lleva oxígeno), y especies reactivas de oxígeno a la luz del intestinal. Sumado a lo anterior, los colonocitos bajo señales pro-inflamatorias realizarían un cambio en su metabolismo hacia una glicólisis anaeróbica, la cual no consume oxígeno permitiendo que este difunda hacia el epitelio intestinal conduciendo así un ambiente favorable para bacterias anaerobias facultativas y aerobias. En este contexto, uno de los componentes de la respuesta inmune innata que parece controlar la población que conforma la microbiota intestinal son los péptidos antimicrobianos (PAMs). Entre los PAMs estudiados en el epitelio colónico se encuentran las Catelicidina (CAMP) y β-defensinas (hBD), los cuales poseen actividad antimicrobiana sobre grupos bacterianos específicos. Modelos murinos que sobreexpresan PAMs muestran una disbiosis con respecto a sus pares silvestres, dando cuenta de la importancia de los PAMs como reguladores de la composición microbiana intestinal. Adicionalmente, investigaciones recientes han demostrado que pacientes con EII poseen una expresión alterada de PAMs con respecto a individuos CTL. En esta línea de pensamiento, esta tesis propuso como hipótesis “El aumento de la población de Proteobacteria observado en la mucosa intestinal en pacientes con EC con respecto a pacientes CU, se asocia con la disminución en la expresión de péptidos antimicrobianos CAMP y hBD 2-4”. Sin embargo, debido al bajo número de muestras que permitieran obtener un RNA íntegro y de calidad para analizar los niveles de expresión de los PAMs CAMP y hBD-2, no fue posible demostrar que nuestros resultados fueron significativos en la correlación con respecto a los phylum bacterianos. En esta condición esta hipótesis no puede ser aceptada ni rechazada. / The highest concentration and diversity of microorganisms belonging to the human microbiota reside in the intestine, establishing a commensal or mutualistic relationship with the host. This relationship can be modified when the microbial structure and composition is altered (dysbiosis). Dysbiosis may be associated to changes in diet, use of antibiotics and to a number of diseases, including inflammatory bowel diseases (IBD) such as Ulcerative Colitis (UC) and Crohn's Disease (CD). Although, due to the easiness to collect them, most of the studies on intestinal microbiota are carried out analyzing stool samples, the adherent microbiota of the colon is representative of the microbial community which co-evolves with the host, interacting directly with the immune system, during the course of the disease. Considering the above, the aim of this thesis was to characterize the adherent microbiota of individuals suffering IBD by means of massive sequencing analysis. Samples (biopsies) were obtained from Chilean and Spanish individuals (n = 66) diagnosed with CD, UC, and control (CTL). Our results showed significant differences between the relative abundance of phyla Proteobacteria and Firmicutes among individuals with IBD and CTL but no differences were observed when comparing the microbiota of individuals with UC and CD. Unlike the studies based on stool samples, in which individuals with IBD are classified as unique and defined groups (CD, CU or CTL) in our study individuals with IBD were classified into five different groups according to their microbial composition. Groups IBD-1, IBD-3, IBD-2 and IBD-5 contained only individuals with CD and UC, presenting an enrichment of phyla Bacteroidetes (34.5%) and Proteobacteria (75.4%) and Operational Phylogenetic Units (OPUs) affiliated with bacteria Ruminococcus gnavus (9.75%) ;Cupriavidus necator / Ralstonia pickettii (6.60%); Brevundimonas diminuta / B revundimonas vancanneytii (5.87%) and Klebsiella oxytoca (32.16%). Group IBD-4 contained individuals with IBD and CTL showing an enrichment of phylum Firmicutes (59.85%) and OPUs affiliated with Faecalibacterium prausnitzii (14.67%), (bacterium characteristic of healthy individuals). In addition to the above, individuals belonging to groups IBD-3, IBD-2 and IBD-5 showed abundances between 12.74 to 55.60% of OPUs affiliated to anaerobic or facultative bacteria, and abundances of 4.25% to 9.68% of OPUs affiliated to obligate aerobes. On the contrary, groups IBD-4 and IBD-1 showed abundances of 41.21% to 45.3% of OPUs affiliated with obligated anaerobic bacteria and abundances close to 1.5% of OPUs affiliated to obligated aerobic bacteria. In addition, correlation analyzes showed negative associations between facultative anaerobic and aerobic OPUs (indicators of individuals with IBD belonging to groups IBD-1, IBD-2, IBD-3, IBD-5) with those obligated anaerobic OPUs (indicators of IBD-4). This kind of correlation exemplifies competition relationships (exclusion) between these bacteria, possibly due to the environmental conditions of the intestine, i.e. an increase in oxygen levels during the process of inflammation. These results are consistent with the "oxygen hypothesis" which proposes that in/under conditions of chronic inflammation, causing the release of oxygen carrying hemoglobin in the intestinal mucosa and reactive oxygen species in the intestinal lumen. In addition, colonocytes under pro-inflammatory signals shift their metabolism towards an oxygen consuming anaerobic glycolysis, increasing epithelial oxygenation which leads to a favorable environment for facultative and aerobic bacteria. One of the components of the innate immune response that seems to control the microbial population are the antimicrobial peptides (AMPs). Among the AMPs studied in the colonic epithelium, Cathelicidin (CAMP) and β-defensins (hBD), which have antimicrobial activity on specific bacterial groups, can be mentioned. Murine models overexpressing AMPs showed a dysbiosis when compared to their wild type mates, revealing the importance of AMPs as regulators of the intestinal microbial composition. Additionally, recent research showed that patients with IBD have an altered expression of AMPs when compared to CTL individuals. In this context, this thesis proposed the following hypothesis: "The increase in the population of Proteobacteria observed in the intestinal mucosa in patients with CD when compared to patients with UC is associated with the decrease in the expression of antimicrobial peptides CAMP and hBD 2-4". However, due to the low number of samples that allowed to obtain a high-quality RNA to analyze the levels of expression of the CAMP and hBD-2 MAPs, it was not possible to demonstrate that our results were significant in the correlation of MAPs with bacterial phyla. In this condition this hypothesis cannot be accepted or rejected. / Fundación Maria Ghilardi, beca para estudios de postgrado durante el año 2013, Comisión Nacional de Ciencia y Tecnología (CONICYT-21140975), beca para estudios de Doctorado (años 2014-2017) y FONDECYT 1161161. / 15 de julio 2019

Objetivo: Tipificar y comparar las microbiotas del arándano “Vaccinium corymbosum” durante variantes de fermentación ácido láctica y realizar la verificación de potenciales sinergias con la microbiota intestinal humana según bibliografía científica. Metodología: El siguiente estudio es de tipo de investigación básica en microbiología, biología molecular y bioquímica in vitro como in vivo. Dicha investigación se realizará en “un ambiente controlado” y busca comparar la presencia de microorganismos a partir de su información genética.

SIBO (Small Intestinal Bacterial Overgrowth) är ett tillstånd där tunntarmen koloniseras av bakterier som normalt finns i tjocktarmen. SIBO utvecklas när de normala homeostatiska mekanismerna som kontrollerar enteriska bakteriepopulationen störs. I tunntarmen ska det finnas väldigt liten mängd bakterier medan i tjocktarmen bör det finnas mycket större mängder bakterier. När bakterierna tar sig in i tunntarmen, resulterar det i SIBO. Denna bakteriella obalans i tunntarmen kan orsaka bland annat uppblåsthet, diarré och magsmärta, förstoppning och försämrat upptag av vitaminer och näringsämnen. Att behandla den underliggande orsaken bakom SIBO är det första steget i behandlingen och om detta inte räcker till, är antibiotikabehandlingen nästa steg. Syftet med denna litteraturstudie var att undersöka hur effektiv Rifaximin är vid behandling av bakteriell överväxt i tunntarmen (SIBO). Arbetet är en litteraturstudie och de vetenskapliga artiklarna är hämtade från databasen Pubmed. I detta arbete har fem studier analyserats. Studie I visade att högdosbehandling med rifaximin gav signifikant ökad behandlingseffekt jämfört med lågdosbehandling hos IBS-patienter. Studie II visade att kombination av amoxicillin och rifaximin kan vara en effektiv förstahandsbehandling för patienter som har både SIBO och H. pylori infektion. Studie III bekräftade att SIBO är underdiagnoserat hos Cystisk fibros patienter och är relaterad till en dålig näringsstatus. Rifaximin är en effektiv behandling av SIBO hos patienter som har Cystisk fibros. Studie IV visade att kombinationen av rifaximin tillsammans med hydrolyserat guargummi verkar vara mer effektivt vid utrotning av SIBO jämfört med enbart rifaximin hos SIBO patienter. Studie V studerade  rifaximinbehandlade IBS-patienter och fann att rifaximinbehandling var associerad med acceleration av kolontransitering samt hade svag påverkan på förändringar i mikrobiell artrikedom i feces. Baserat på de fem studierna föreligger det skäliga bevis att behandling med rifaxamin är en effektiv behandling vid SIBO. Mer forskning och studier behövs för att kunna bestämma den bästa dosen samt utvärdera rifaximin i kombination med andra läkemedel. / SIBO (Small Intestinal Bacterial Overgrowth) is a condition where the small intestine is colonized by bacteria normally found in the large intestine. SIBO develops when the normal homeostatic mechanisms controlling the enteric bacterial population are disrupted. In the small intestine, there should be very small number of bacteria while in the large intestine there should be much larger number of bacteria. When the bacteria colonizes the small intestine, it results in SIBO. This bacterial imbalance in the small intestine can cause bloating, diarrhea and stomach pain, constipation and impaired absorption of vitamins and nutrients. Treating the underlying cause of SIBO is the first step in the treatment and if this is not enough, antibiotic treatment is the next step. The purpose of this literature study was to investigate the effectiveness of Rifaximin in treatment of bacterial overgrowth in the small intestine (SIBO). The study is a literature study where the scientific articles were obtained from the database Pubmed. In this literature study, five studies have been analyzed. Study I showed that high-dose treatment with rifaximin significantly increased treatment efficacy compared to low-dose treatment. Study II showed that a combination of amoxicillin and rifaximin can be an effective first-line treatment for patients who have both SIBO and H. pylori infection. Study III confirmed that SIBO is underdiagnosed in CF patients, related to poor nutritional status. Rifaximin is an effective treatment for SIBO in patients who have CF. Study IV also showed a combination treatment where rifaximin together with hydrolyzed guar gum appears to be more effective in eradicating SIBO compared to rifaximin alone. Study V studied rifaximin-treated IBS patients, rifaximin treatment was associated with acceleration of colon transit, and a weak influence on changes in microbial species richness in faeces. Based on the five studies, there is reasonable evidence that a treatment with rifaximin is an effective treatment for SIBO. However, more research and studies are needed to determine the best dose and also rifaximin in combination with other drugs.

Wolbachia is a vertically transmitted, obligate intracellular bacterium infecting ~40% of all known species of arthropods, as well as filarial nematodes. The nature of Wolbachia-host interactions ranges from reproductive parasitism to increased fecundity and pathogen protection. Wolbachia reduces the ability of mosquitoes to transmit human pathogens, which is being explored as a novel method for the control of vector-borne diseases like Dengue and Zika. The mechanisms of Wolbachia blocking the transmission of these diseases are not fully understood. There are studies indicating that Wolbachia-induced changes in the insect immunity could block the virus, however there is no consensus in the literature. A necessary step in the transmission of these diseases is the viral entry into the insect vector. This occurs trough the gut epithelium, highlighting the importance of understanding the interaction of this tissue with microorganisms. We have recently shown that Wolbachia colonizes the Drosophila gut epithelium and affects the gut microbiome composition. Wolbachia’s presence did not affect the gene expression of immune effector molecules from the main regulators of gut immunity, Imd and ROS pathways. Our understanding of the mechanisms of Wolbachia’s colonization of the gut epithelium and modulation of gut microbiome are still very limited. This work characterizes Wolbachia’s kinetics of colonization in Drosophila midguts. Imaging analysis revealed that Wolbachia colonizes adult and larval midguts in different patterns. We have also characterized a preferential colonization in specific adult midgut sub-regions. We observed that Wolbachia patches are confined to specific midgut subregions, in a pattern similar to the arrangement of intestinal stem cell (ISC) clones. These results led us to hypothesize that Wolbachia colonizes Drosophila midguts by infecting intestinal progenitor cells and spreading vertically to their progeny with limited lateral transmission between neighboring cells. We provide evidence to support this hypothesis by showing that Wolbachia is present in intestinal progenitor cells in all stages of the fly’s life cycle as well as by analyzing the infection status of ISC clones and differentiated cells surrounding ISCs. Finally, we found that ISC proliferation is reduced by the intracellular presence of Wolbachia, which also decreases ISC tumor incidence triggered by the downregulation of Notch signaling specifically in ISCs. These findings will aid in our understanding of Wolbachia tropisms and its phenotypic consequences. It has been shown that in the Wolbachia wMelPop strain excessive growth of intracellular bacteria leads to damage to the host cell, suggesting a mechanism of controlling intracellular growth in other strains. To better understand the molecular mechanisms behind Wolbachia-Drosophila interactions, we turned to the gonads, as Wolbachia colonization of these tissues has been well characterized. We chose to investigate the interplay between Reactive Oxygen Species (ROS) and Wolbachia, as intracellular ROS could regulate bacterial density but also be affected by Wolbachia and play a role in symbiont-related phenotypes. Using direct and indirect measurements of ROS, we show that the pathogenic strain wMelPop increases ROS in the germarium, while the symbiotic strains wMel and wMelCS reduce ROS in the terminal filaments. None of the Wolbachia strains tested affected ROS levels in the testes. In addition, genetically altering ROS levels in the germline or systemically in the fly did not affect Wolbachia levels in the ovaries. We conclude that ROS does not significantly affect Wolbachia in the fruit fly gonads.

β-Glucans have beneficial health effects due to their immune modulatory properties. Oral administration of β-glucans affects tumour growth, microbial infection, sepsis, and wound healing. We hypothesized that pre-treatment with orally delivered soluble and particulate β-glucans could ameliorate the development of aggravate dextran sulfate sodium (DSS) induced intestinal inflammation. To study this, mice were orally pre-treated with β-glucans for 14 days. We tested curdlan (a particulate β-(1,3)-glucan), glucan phosphate (a soluble β-(1,3)-glucan), and zymosan (a particle made from Saccharomyces cerevisiae, which contains around 55% β-glucans). Weight loss, colon weight, and feces score did not differ between β-glucan and vehicle treated groups. However, histology scores indicated that β-glucan-treated mice had increased inflammation at a microscopic level suggesting that β-glucan treatment worsened intestinal inflammation. Furthermore, curdlan and zymosan treatment led to increased colonic levels of inflammatory cytokines and chemokines, compared to vehicle. Glucan phosphate treatment did not significantly affect cytokine and chemokine levels. These data suggest that particulate and soluble β-glucans differentially affect the intestinal immune responses. However, no significant differences in other clinical colitis scores between soluble and particulate β-glucans were found in this study. In summary, β-glucans aggravate the course of dextran sulfate sodium (DSS)-induced intestinal inflammation at the level of the mucosa.

The role of dietary phytate (inositol hexaphosphate) in the regulation of intestinal mucosa phytase was investigated in chicks. Seven-day-old chicks were grouped by weight into six blocks of three cages with six birds per cage. Three purified diets [a chemically defined casein diet, a chemically defined casein diet plus sodium phytate (20 g/kg diet) and a chemically defined casein diet plus sodium phytate (20 g/kg diet) and microbial phytase (1000 units/kg diet)] were randomly assigned to cages within each block. Chicks were fed experimental diets from 8 to 22 days of age then killed, and duodenal mucosa and left tibia removed. Phytase activity in duodenal mucosa, growth performance and bone ash content were determined. Addition of phytate to the chemically defined casein diet reduced (p < 0.05) the Vmax of the duodenal brush border phytase, but the Km of the enzyme was not affected. Addition of phytate also reduced (p < 0.05) weight gain, feed intake, feed efficiency and percentage ash. Addition of microbial phytase fully restored the feed efficiency (p < 0.05), but Vmax and body weight gain were only partially restored (p < 0.05). In conclusion, it would seem that dietary phytates non-competitively inhibit intestinal mucosa phytase.

No description available.