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PubMed2004

Microbial-gut interactions in health and disease. Prebiotics.

In nutritional sciences there is much interest in dietary modulation of the human gut. The gastrointestinal tract, particularly the colon, is very heavily populated with bacteria. Most bacteria are benign; however, certain gut species are pathogenic and may be involved in the onset of acute and chronic disorders. Bifidobacteria and lactobacilli are thought to be beneficial and are common targets for dietary intervention. Prebiotic is a non-viable food ingredient selectively metabolized by beneficial intestinal bacteria. Dietary modulation of the gut microflora by prebiotics is designed to improve health by stimulating numbers and/or activities of the bifidobacteria and lactobacilli. Having an 'optimal' gut microflora can increase resistance to pathogenic bacteria, lower blood ammonia, increase stimulation of the immune response and reduce the risk of cancer. This chapter examines how prebiotics are being applied to the improvement of human health and reviews the scientific evidence behind their use.

Bifidobacterium↗
PubMed2004

Microbial-gut interactions in health and disease. Immune responses.

The indigenous bacterial microflora colonize the gut at birth and remain there throughout life. Approximately 10(14) bacteria are present in the ileum and colon and they are clearly immunogenic. The evidence is strong that the vast majority of IgA plasma cells in normal human gut are responding to the antigens of the flora, and although the flora is also responsible for producing the large numbers of T cells which are present in the gut of healthy individuals, the types of T cell response which the flora elicits are less well understood. A major challenge for the immune system is to distinguish between the antigens of the flora and the antigens of pathogens. There is also a growing realization that the normal flora can also influence gene expression in antigen-presenting cells in the gut and so set the context in which T cells respond to food antigen and vaccines.

Animals↗
PubMed2004

Microbial-gut interactions in health and disease. Mucosal immune responses.

The host gastrointestinal tract is exposed to countless numbers of foreign antigens and has embedded a unique and complex network of immunological and non-immunological mechanisms, often termed the gastrointestinal 'mucosal barrier', to protect the host from potentially harmful pathogens while at the same time 'tolerating' other resident microbes to allow absorption and utilization of nutrients. Of the many important roles of this barrier, it is the distinct responsibility of the mucosal immune system to sample and discriminate between harmful and beneficial antigens and to prevent entry of food-borne pathogens through the gastrointestinal (GI) tract. This system comprises an immunological network termed the gut-associated lymphoid tissue (GALT) that consists of unique arrangements of B cells, T cells and phagocytes which sample luminal antigens through specialized epithelia termed the follicle associated epithelia (FAE) and orchestrate co-ordinated molecular responses between immune cells and other components of the mucosal barrier. Certain pathogens have developed ways to bypass and/or withstand defence by the mucosal immune system to establish disease in the host. Some 'opportunistic' pathogens (such as Clostridium difficile) take advantage of host or other factors (diet, stress, antibiotic use) which may alter or weaken the response of the immune system. Other pathogens have developed mechanisms for invading gastrointestinal epithelium and evading phagocytosis/destruction by immune system defences. Once cellular invasion occurs, host responses are activated to limit local mucosal damage and repel the foreign influence. Some pathogens (Shigella spp, parasites and viruses) primarily establish localized disease while others (Salmonella, Yersinia, Listeria) use the lymphatic system to enter organs or the bloodstream and cause more systemic illness. In some cases, pathogens (Helicobacter pylori and Salmonella typhi) colonize the GI tract or associated lymphoid structures for extended periods of time and these persistent pathogens may also be potential triggers for other chronic or inflammatory diseases, including inflammatory bowel disease and malignancies. The ability of certain pathogens to avoid or withstand the host's immune assault and/or utilize these host responses to their own advantage (i.e. enhance further colonization) will dictate the pathogen's success in promoting illness and furthering its own survival.

Bacteria↗
PubMed2004

Microbial-gut interactions in health and disease. Irritable bowel syndrome.

The intestinal microbiota interacts with several aspects of gastrointestinal function that may affect the expression or progression of disease. For example, a role for bacterial metabolism of bile acids and food has been linked to colorectal cancer development. Studies have also shown a potential role of the intestinal microbiota in the modulation of inflammation in the intestine and joints. Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. Early studies in axenic mice demonstrated gross morphological abnormalities and gut motor dysfunction related to the absence of a normal microflora, raising the possibility that shifts in commensal bacterial populations could play a role in the development of altered motility states including functional disorders of the gut. This chapter concentrates on the experimental evidence for a role of intestinal microbiota and the potential therapeutic value of probiotics in functional diseases such as irritable bowel syndrome.

Animals↗
PubMed2004

Microbial-gut interactions in health and disease. Progress in enteric vaccine development.

Enteric infections resulting in diarrhoea are among the most important causes of morbidity and mortality, particularly in children in developing countries. They are also a common cause of disease among travellers to Africa, Asia and Latin America. Recently, effective, live and inactivated oral and parenteral vaccines against some of the most severe enteric infections-cholera and typhoid fever-have been licensed in several countries. Different candidate vaccines against rotavirus, Shigella and ETEC diarrhoea have also been developed and tested for safety and immunogenicity in developed as well as in developing countries. The protective efficacy of several of these vaccines has also been tested, either in human volunteer challenge studies or in field trials. In this chapter we describe the properties and availability of the recently licensed vaccines and present an update on the diverse efforts being made to achieve new or improved vaccines against the most prevalent enteropathogens.

Cholera↗
PubMed2004

Analysis of a novel class of predictive microbial growth models and application to coculture growth.

In this paper, a novel class of microbial growth models is analysed. In contrast with the currently used logistic type models (e.g., the model of Baranyi and Roberts [Baranyi, J., Roberts, T.A., 1994. A dynamic approach to predicting bacterial growth in food. International Journal of Food Microbiology 23, 277-294]), the novel model class, presented in Van Impe et al. (Van Impe, J.F., Poschet, F., Geeraerd, A.H., Vereecken, K.M., 2004. Towards a novel class of predictive microbial growth models. International Journal of Food Microbiology, this issue), explicitly incorporates nutrient exhaustion and/or metabolic waste product effects inducing stationary phase behaviour. As such, these novel model types can be extended in a natural way towards microbial interactions in cocultures and microbial growth in structured foods. Two illustrative case studies of the novel model types are thoroughly analysed and compared to the widely used model of Baranyi and Roberts. In a first case study, the stationary phase is assumed to be solely resulting from toxic product inhibition and is described as a function of the pH-evolution. In the second case study, substrate exhaustion is the sole cause of the stationary phase. Finally, a more complex case study of a so-called P-model is presented, dealing with a coculture inhibition of Listeria innocua mediated by lactic acid production of Lactococcus lactis.

Coculture Techniques↗
PubMed2006

Interactions between microbial iron reduction and metal geochemistry: effect of redox cycling on transition metal speciation in iron bearing sediments.

Microbial iron reduction is an important biogeochemical process that can affect metal geochemistry in sediments through direct and indirect mechanisms. With respectto Fe(III) (hydr)oxides bearing sorbed divalent metals, recent reports have indicated that (1) microbial reduction of goethite/ferrihydrite mixtures preferentially removes ferrihydrite, (2) this process can incorporate previously sorbed Zn(II) into an authigenic crystalline phase that is insoluble in 0.5 M HCl, (3) this new phase is probably goethite, and (4) the presence of nonreducible minerals can inhibit this transformation. This study demonstrates that a range of sorbed transition metals can be selectively sequestered into a 0.5 M HCl insoluble phase and that the process can be stimulated through sequential steps of microbial iron reduction and air oxidation. Microbial reduction experiments with divalent Cd, Co, Mn, Ni, Pb, and Zn indicate that all metals save Mn experienced some sequestration, with the degree of metal incorporation into the 0.5 M HCl insoluble phase correlating positively with crystalline ionic radius at coordination number = 6. Redox cycling experiments with Zn adsorbed to synthetic goethite/ferrihydrite or iron-bearing natural sediments indicate that redox cycling from iron reducing to iron oxidizing conditions sequesters more Zn within authigenic minerals than microbial iron reduction alone. In addition, the process is more effective in goethite/ferrihydrite mixtures than in iron-bearing natural sediments. Microbial reduction alone resulted in a -3x increase in 0.5 M HCl insoluble Zn and increased aqueous Zn (Zn-aq) in goethite/ferrihydrite, but did not significantly affect Zn speciation in natural sediments. Redox cycling enhanced the Zn sequestration by approximately 12% in both goethite/ferrihydrite and natural sediments and reduced Zn-aq to levels equal to the uninoculated control in goethite/ferrihydrite and less than the uninoculated control in natural sediments. These data suggest that in situ redox cycling may serve as an effective method for

Ferric Compounds↗
PubMed2001

Actinide interactions with microbial chelators: the dioxobis[pyridine-2,6-bis(monothiocarboxylato)]uranium(VI) ion.

The title complex, bis(tetraphenylphosphonium) dioxobis(pyridine-2,6-dicarbothioato-O,N,O')uranium(VI), (C(24)H(20)P)(2)[UO(2)(C(7)H(3)NO(2)S(2))(2)], was prepared by reacting two equivalents of pyridine-2,6-bis(monothiocarboxylate) (pdtc) with uranyl nitrate. The geometry of the eight-coordinate U atom is hexagonal bipyramidal, with the uranyl O atoms in apical positions. This is the first reported complex in which this ligand binds a metal through the O and not the S atoms. Principal bond lengths include uranyl lengths of 1.774 (2) A, U--O distances of 2.434 (2) and 2.447 (3) A, and two U--N distances of 2.647 (3) A. The anion lies on an inversion centre.

Actinoid Series Elements↗
PubMed1981

Composting process control based on interaction between microbial heat output and temperature.

Rational composting process control involves the interrelated factors of heat output, temperature, ventilation, and water removal. The heat is released microbially at the expense of organic material; temperature is an effect and, because it is a determinant of microbial activity, it is also a cause of heat output; ventilation supplies oxygen and removes heat, mainly through the vaporization of water; water removal results from heat removal. These relationships were implemented in a field-scale process of static-pile configuration, using a mixture of sewage sludge and wood chips. Heat removal was matched to heat output through a temperature feedback control system, thereby maintaining biologically favorable temperatures. The observations indicate that fundamentally there are two kinds of composting systems: those that are and those that are not temperature self-limiting. The self-limiting system reaches inhibitive temperatures (>60 degrees C) which debilitate the microbial community, suppressing decomposition, heat output, and water removal. In contrast, non-self-limiting temperatures (<60 degrees C) support a robust community, promoting decomposition, heat output, and water removal.

Journal Article↗
PubMed1989

Metal Interactions with Microbial Biofilms in Acidic and Neutral pH Environments.

Microbial biofilms were grown on strips of epoxy-impregnated filter paper submerged at four sites in water contaminated with metals from mine wastes. At two sample stations, the water was acidic (pH 3.1); the other sites were in a lake restored to a near neutral pH level by application of a crushed limestone slurry. During a 17-week study period, planktonic bacterial counts increased from 10 to 10 CFU/ml at all sites. Biofilm counts increased rapidly over the first 5 weeks and then leveled to 10 CFU/cm in the neutral pH system and 10 CFU/cm at the acidic sites. In each case, the biofilms bound Mn, Fe, Ni, and Cu in excess of the amounts adsorbed by control strips covered with nylon filters (pore size, 0.22 mum) to exclude microbial growth; Co bound under neutral conditions but not under acidic conditions. Conditional adsorption capacity constants, obtained graphically from the data, showed that biofilm metal uptake at a neutral pH level was enhanced by up to 12 orders of magnitude over acidic conditions. Similarly, adsorption strength values were usually higher at elevated pH levels. In thin sections of the biofilms, encapsulated bacterial cells were commonly found enmeshed together in microcolonies. The extracellular polymers often contained iron oxide precipitates which generated weak electron diffraction patterns with characteristic reflections for ferrihydrite (Fe(2)O(3) . H(2)O) at d equaling 0.15 and 0.25 nm. At neutral pH levels, these deposits incorporated trace amounts of Si and exhibited a granular morphology, whereas acicular crystalloids containing S developed under acidic conditions.

Journal Article↗
PubMed2001

Microbes and microbial toxins: paradigms for microbial-mucosal interactions I. Pathophysiological aspects of enteric infections with the lumen-dwelling protozoan pathogen Giardia lamblia.

Giardia lamblia is one of the most important causes of waterborne diarrheal disease worldwide, and giardiasis is the most common protozoan infection of the human small intestine. Symptomatic infection is characterized by diarrhea, abdominal pain, and malabsorption, leading to malnutrition and weight loss, particularly in children. The pathogen resides strictly in the lumen of the small intestine, and infection is typically not accompanied by significant mucosal inflammation. Clinical and experimental studies indicate that B cell-dependent host defenses, particularly IgA, are important for controlling and clearing Giardia infection, although B cell-independent mechanisms also contribute to this outcome. In contrast to antigiardial host defenses, much less is known about the pathophysiological mechanisms underlying the clinical symptoms of giardiasis, partly because of the current lack of suitable model systems. In addition to being an important human enteric pathogen, Giardia is an interesting model organism for gaining basic insights into genetic innovations that led to evolution of eukaryotic cells, since it belongs to the earliest diverging eukaryotic lineage known. The completion of the giardial genome project will increase understanding of the basic biology of the protozoan and will help us to better understand host pathogen-interactions as a basis for developing new vaccination and therapeutic strategies.

Animals↗
PubMed2001

Microbes and microbial toxins: paradigms for microbial-mucosal interactions II. The integrated response of the intestine to Clostridium difficile toxins.

Clostridium difficile, the major etiologic factor of antibiotic-associated diarrhea and colitis, mediates its effects by releasing two large protein exotoxins, toxins A and B. A major toxin effect is related to the disassembly of actin microfilaments, leading to impairment of tight junctions in human colonocytes. The mechanism of actin disaggregation involves monoglucosylation of the signaling proteins Rho A, Rac, and Cdc 42, which control stress fiber formation directly by toxins A and B. An important aspect of C. difficile infection is the acute necroinflammatory changes seen in patients with pseudomembranous colitis. The early mechanism of toxin-mediated inflammation involves toxin effects on cellular mitochondria, release of reactive oxygen species, and activation of mitogen-activated protein kinases and the transcription factor nuclear factor-kappaB. Injection of toxin A into animal intestine triggers secretion of fluid and intestinal inflammation characterized by epithelial cell destruction and neutrophil activation. A critical feature of C. difficile enterotoxicity is communication between enterocytes and lamina propria nerves, macrophages, and mast cells mediated via release of neuropeptides and proinflammatory cytokines.

Acute-Phase Proteins↗
PubMed2001

Microbes and microbial toxins: paradigms for microbial-mucosal interactions III. Shigellosis: from symptoms to molecular pathogenesis.

Interaction of Shigella flexneri with epithelial cells includes contact of bacteria with the cell surface and release of Ipa proteins through a specialized type III secreton. A complex signaling process involving activation of small GTPases of the Rho family and c-src causes major rearrangements of the subcortical cytoskeleton, thereby allowing bacterial entry by macropinocytosis. After entry, shigellae escape to the cell cytoplasm and initiate intracytoplasmic movement through polar nucleation and assembly of actin filaments caused by bacterial surface protein IcsA, which binds and activates neuronal Wiskoff-Aldrich syndrome protein (N-WASP), thus inducing actin nucleation in an Arp 2/3-dependent mechanism. Actin-driven motility promotes efficient colonization of the host cell cytoplasm and rapid cell-to-cell spread via protrusions that are engulfed by adjacent cells in a cadherin-dependent process. Bacterial invasion turns infected cells to strongly proinflammatory cells through sustained activation of nuclear factor-kappaB. A major consequence is interleukin (IL)-8 production, which attracts polymorphonuclear leukocytes (PMNs). On transmigration, PMNs disrupt the permeability of this epithelium and promote its invasion by shigellae. At the early stage of infection, M cells of the follicle-associated epithelium allow bacterial translocation. Subsequent apoptotic killing of macrophages in a caspase 1-dependent process causes the release of IL-1beta and IL-18, which accounts for the initial steps of inflammation.

Dysentery, Bacillary↗
PubMed2001

Microbes and microbial toxins: paradigms for microbial-mucosal interactions. VI. Entamoeba histolytica: parasite-host interactions.

The protozoan intestinal parasite Entamoeba histolytica remains a significant cause of morbidity and mortality worldwide. E. histolytica causes two major clinical syndromes, amebic colitis and amebic liver abscess. Recent advances in the development of in vitro and in vivo models of disease, new genetic approaches, the identification of key E. histolytica virulence factors, and the recognition of crucial elements of the host response to infection have led to significant insights into the pathogenesis of amebic infection. E. histolytica virulence factors include 1) a surface galactose binding lectin that mediates E. histolytica binding to host cells and may contribute to amebic resistance to complement, 2) amebapores, small peptides capable of lysing cells, which may play a role in killing intestinal epithelial cells, hepatocytes, and host defense cells, and 3) a family of secreted cysteine proteinases that play a key role in E. histolytica tissue invasion, evasion of host defenses, and parasite induction of gut inflammation. Amebae can both lyse host cells and induce their suicide through programmed cell death. The host response is also an important factor in the outcome of infection, and neutrophils may play a key role in contributing to the tissue damage seen in amebiasis and in controlling amebic infection.

Animals↗
PubMed2001

Microbes and microbial toxins: paradigms for microbial-mucosal interactions. VII. Enteropathogenic Escherichia coli: physiological alterations from an extracellular position.

Enteropathogenic Escherichia coli (EPEC) is primarily associated with infantile diarrhea in developing countries. This intriguing pathogen exerts numerous physiological effects on its host target tissue, the intestinal epithelium, all from an extracellular location. Expression of a type III secretory apparatus allows this organism to transfer bacterial effector molecules directly into host cells. As a result of EPEC attachment to and/or translocation of proteins into intestinal epithelial cells, many signaling cascades are activated. Ultimately, host functions are perturbed, including alteration of ion transport, disruption of the tight junction barrier, and activation of the inflammatory response.

Diarrhea↗