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Early interactions between Entamoeba histolytica and mucosal cellsKammanadiminti, Srinivas Jagannadha. January 2006 (has links)
The pathogenesis of the enteric protozoan parasite Entamoeba histolytica remains poorly understood. Moreover, the host responses during the early periods of interaction in the gut remain to be clarified. In this study I investigated the cell specific responses to the parasite and the importance of cross talk between epithelial-immune cells that could potentially influence the outcome of infection, with a central focus on Nuclear factor (NF)-kappaB. NF-kappaB is a ubiquitous transcription factor that plays a critical role in mucosal inflammation and its regulation by E. histolytica has not been studied so far. Gal-lectin is a well characterized parasite virulence factor and vaccine candidate. I first characterized the interactions between Gal-lectin and macrophages and found that several proinflammatory genes are upregulated as early as 2h. The Gal-lectin activated NF-kappaB and up-regulated Toll like receptor-2 expression in an NF-kappaB- and p38 Mitogen Activated Protein (MAP) kinase-dependent manner. As intestinal epithelial cells (IEC) form the first line of active host defense against mucosal pathogens, I determined the interaction between ameba soluble proteins and naive IEC. I observed that the parasite could elicit a chemokine response via activation of PI3 kinase and phosphorylation of p65 subunit to induce monocyte chemoattractant protein-1. The consequent recruitment of immune cells could be responsible for colonic inflammation. Finally, I made the novel observation that in macrophage-primed IEC, ameba proteins elicited a cytoprotective stress response. Using a combination of siRNA and over expression studies, I demonstrated that amebic proteins increased the expression and phosphorylation of Heat shock protein (Hsp) 27 thereby enhancing its association with and subsequent inhibition of Inhibitory kappaB kinase (IKK). The resulting inhibition of NF-kappaB could be a potential mechanism that explains the absence of inflammation in the majority of infected individuals. Taken together, the findings of this study open up a new facet in the pathogenesis of amebiasis and unravel a novel paradigm to study host-parasite interactions in the gut.
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Auxiliary cofactors in the metabolism of citrate by yeast (i) ; Biochemical studies of intestinal mucins (ii)Whitehouse, M. W. January 1955 (has links)
The properties of factors present in boiled yeast juice which stimulate the oxidative breakdown of citrate in baker's yeast have been investigated. The activity has been shown to reside predominantly in the nucleotide fractions (i.e., pyridine codehydrogenases) and to a lesser extent in the ammonium salts present in whole yeast cells. The activity of the Citrate Oxidation Factor (COF) concentrated from yeast extracts and described by Foulkes (Biochem. J. 54 323 (1953)) was attributable entirely to the ammonium content of COF preparations. This activating effect of ammonium ions is accompanied by their removal from the assay system and the simultaneous production of glutamic acid. Correlation of the uptake of ammonium ion with the increased citrate metabolism indicates that the activity of the ammonium salts lies in their ability to promote the reductive amination of α-oxoglutarate. The mechanism(s) whereby this serves to stimulate the further breakdown of citrate to oxoglutarate involves the mediation of the pyridine codehydrogenases (DPN, TPN). These findings are discussed in relation to the known functioning of individual stains of the tricarboxylic acid cycle and to possible alternative pathways for the oxidation of citrate in yeast.
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Early interactions between Entamoeba histolytica and mucosal cellsKammanadiminti, Srinivas Jagannadha. January 2006 (has links)
No description available.
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Intestinal cell kinetics : modulation caused by age, gender and microbial status in rats and mice : an experimental study in germfree, conventional and Lactobacillus rhamnosus GG or Clostridium difficile, mono-associated animals /Banasaz, Mahnaz, January 2002 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 4 uppsatser.
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Activation of the mucosal immune system and growth of the small intestine at weaning / by Fiona Marie Thompson.Thompson, Fiona Marie January 1994 (has links)
Contains errata sheet in back pocket. / Bibliography: leaves 167-211. / xviii, 211, [8] leaves, [4] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Explores the hypothesis that growth of the small intestine at weaning is promoted by an activated mucosal immune system in the gut. Tests by observing rats, guinea pigs and human infants. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1995?
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Modulation of intestinal epithelial cell-mediated defence responses bymetabolic products of Lactobacillus rhamnosus GG and Escherichia coliNissle 1917Chen, Zhijian, 陈智健 January 2012 (has links)
Probiotics are defined as live microorganisms that confer beneficial effects to health when administered in a sufficient amount. In previous studies about the beneficial effects of probiotic bacteria to health, particularly in the fields of intestinal mucosa defence responses, specific probiotics, in a strain-dependent manner, show some potential to reinforce the integrity of intestinal epithelium and/or regulate some immune components. However, the mechanisms involved in the interactions between probiotics or bioactive components of probiotics with the intestinal epithelium are still not yet clearly defined or systematically studied. Among all possible routes of modulation by probiotics of intestinal epithelial cell–mediated defence responses, modulations of mucin and trefoil factor expression as well as the cytokine profiles are important components of the innate and adaptive mucosal immune responses of the intestinal epithelial cells and are considered to play important role in the intestinal defence responses against pathogenic bacteria.
This thesis examined and characterized the in vitro modulation effects by metabolic products of two commonly studied probiotics bacterial strains, Lactobacillus rhamnosus GG (LGG) and Escherichia coli Nissle 1917 (EcN), on the intestinal epithelial cell-mediated defence responses. It was found that the metabolic products of EcN decreased the transcriptional levels of secretory mucins MUC5AC, MUC5B and MUC2 while LGG metabolic products only down-regulated that of MUC5AC. In partial agreement with the reduction of mucin gene expression levels, intracellular MUC5B and MUC2 mucin expression was reduced by EcN metabolic products and MUC5AC and MUC2 by the metabolic products of LGG. In contrast, the extracellular MUC5AC and MUC2 mucin expression tended to increase upon the effects of both LGG and EcN metabolic products, which might result from accumulative effects of the modulation on extracellular mucin secretion during the time of treatment or the differential responsiveness of cellular mucin gene and protein expression upon stimulation. The expression of trefoil factor 3 in both gene and protein levels upon the effects of EcN metabolic products while those of LGG enhanced the transcriptional but not protein level. As for the modulation of cytokine profiles, LGG metabolic products mainly influence the secretion of anti-inflammatory cytokines such as IL-4, IL-5 and IL-10 in a moderate manner while EcN metabolic products exerted broad pro-inflammatory potential to the intestinal epithelial cells by inducing the secretion of pro-inflammatory cytokines such as IL-8, MCP-1, TGF-α, TNF-α and GM-CSF, which indicated that the metabolic products of LGG and EcN might initiate differential signaling pathway to influence the intestinal epithelial adaptive immune responses.
To conclude, the present research provides evidence to substantiate that LGG and EcN display differential modulation mechanisms of the intestinal epithelial cell-mediated defence responses that involve intestinal-cell mediated mucin and trefoil factor secretion as well as pro- and anti-inflammatory cytokine expression. / published_or_final_version / Biological Sciences / Master / Master of Philosophy
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Nitric oxide in inflammatory bowel disease /Ljung, Tryggve, January 2003 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.
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Signaling and lineage relationships during intraepithelial lymphocyte development /Page, Stephanie T., January 1997 (has links)
Thesis (Ph. D.)--University of Washington, 1997. / Vita. Includes bibliographical references (leaves [78]-93).
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Intestinal permeability a parameter of mucosal dysfunction /Lundin, Pål. January 1997 (has links)
Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.
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Evaluation of mucosal damage and recovery in the gastrointestinal tract of rats by penetration enhancersNarkar, Yogeeta. January 2006 (has links)
Thesis (Ph.D.)--University of Wisconsin--Madison, 2006 / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (p. 186-199).
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