Academic literature on the topic 'Mucosal surfaces'

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Journal articles on the topic "Mucosal surfaces"

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Brown, T. A. "Immunity at Mucosal Surfaces." Advances in Dental Research 10, no. 1 (April 1996): 62–65. http://dx.doi.org/10.1177/08959374960100011201.

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The mucosae form a barrier between our bodies and a hostile external environment. Diseases and extrinsic factors which impair mucosal function may lead to serious consequences. The mucosal immune system is the primary mediator of specific immunity at mucosal surfaces. As such, it is responsible for maintaining homeostasis and for defense against both overt and opportunistic pathogens. For this reason, it is also the target of many new vaccine strategies for the induction of mucosal immunity. This brief review will examine the mucosal immune system, its role in maintaining the integrity of the mucosa, and some of the strategies aimed at enhancing specific immunity.
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Dougan, Gordon, Marjan Ghaem–Maghami, Derek Pickard, Gad Frankel, Gill Douce, Simon Clare, Sarah Dunstan, and Cameron Simmons. "The immune responses to bacterial antigens encountered in vivo at mucosal surfaces." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1397 (May 28, 2000): 705–12. http://dx.doi.org/10.1098/rstb.2000.0610.

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Mammals have evolved a sophisticated immune system for handling antigens encountered at their mucosal surfaces. The way in which mucosally delivered antigens are handled influences our ability to design effective mucosal vaccines. Live attenuated derivatives of pathogens are one route towards the development of mucosal vaccines. However, some molecules, described as mucosal immunogens, are inherently immunogenic at mucosal surfaces. Studies on mucosal immunogens may facilitate the identification of common characteristics that contribute to mucosal immunogenicity and aid the development of novel, non–living mucosal vaccines and immunostimulators.
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Oldham, Geoffrey. "Aspects of Immunology of the Gut and Rotavirus Infection." Proceedings of the British Society of Animal Production (1972) 1993 (March 1993): 32. http://dx.doi.org/10.1017/s0308229600023618.

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The major portal of entry for most pathogenic microorganisms is the mucosal surface. It seems reasonable therefore that the host in its turn should possess substantial immune defences at the mucosae to provide protection against these insults. Enteric infections usually result in at least some degree of specific protection against a subsequent infection with the same organism. However artificial induction of mucosal immunity has proved difficult. Clearly, as yet, we do not have a full understanding of the inductive events involved in the generation of mucosal immune responses or the immune mechanisms operating at mucosal surfaces. In this paper I will attempt to briefly review the main aspects of mucosal immunity concentrating on the gut as the model mucosal surface.
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Feng, Fengling, Ziyu Wen, Jiaoshan Chen, Yue Yuan, Congcong Wang, and Caijun Sun. "Strategies to Develop a Mucosa-Targeting Vaccine against Emerging Infectious Diseases." Viruses 14, no. 3 (March 3, 2022): 520. http://dx.doi.org/10.3390/v14030520.

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Numerous pathogenic microbes, including viruses, bacteria, and fungi, usually infect the host through the mucosal surfaces of the respiratory tract, gastrointestinal tract, and reproductive tract. The mucosa is well known to provide the first line of host defense against pathogen entry by physical, chemical, biological, and immunological barriers, and therefore, mucosa-targeting vaccination is emerging as a promising strategy for conferring superior protection. However, there are still many challenges to be solved to develop an effective mucosal vaccine, such as poor adhesion to the mucosal surface, insufficient uptake to break through the mucus, and the difficulty in avoiding strong degradation through the gastrointestinal tract. Recently, increasing efforts to overcome these issues have been made, and we herein summarize the latest findings on these strategies to develop mucosa-targeting vaccines, including a novel needle-free mucosa-targeting route, the development of mucosa-targeting vectors, the administration of mucosal adjuvants, encapsulating vaccines into nanoparticle formulations, and antigen design to conjugate with mucosa-targeting ligands. Our work will highlight the importance of further developing mucosal vaccine technology to combat the frequent outbreaks of infectious diseases.
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Parrott, D. M. V. "Mucosal immunity and infections at mucosal surfaces." Immunology Today 10, no. 4 (April 1989): 138. http://dx.doi.org/10.1016/0167-5699(89)90248-x.

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Gryboski, Joyce D. "Mucosal immunity and infections at mucosal surfaces." Gastroenterology 96, no. 3 (March 1989): 952–53. http://dx.doi.org/10.1016/0016-5085(89)90935-9.

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Russell, Michael W., and Pearay L. Ogra. "Mucosal Decisions: Tolerance and Responsiveness at Mucosal Surfaces." Immunological Investigations 39, no. 4-5 (January 1, 2010): 297–302. http://dx.doi.org/10.3109/08820131003729927.

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Smith, Phillip D., and Ruizhong Shen. "Target Cells for HIV-1/SIV Infection in Mucosal Tissue." Current Immunology Reviews 15, no. 1 (April 12, 2019): 28–35. http://dx.doi.org/10.2174/1573395514666180531072126.

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The mucosal surfaces of the genital and gastrointestinal tracts are the routes by which HIV-1 is acquired, excluding persons infected parenterally. Identification of the mucosal target cells and the receptors by which HIV-1 enters these cells is fundamental to elucidating the biology of HIV-1 transmission. The mucosal target cells include epithelial cells, dendritic cells, Langerhans cells, CD4+ T-cells, macrophages and even mast cells, but the contribution of each cell type is highly dependent on the mucosal surface - genital versus gastrointestinal. Importantly, mucosal target cells may also play key roles in the immunobiology and latency of HIV-1 infection. Given the pivotal role of mucosal cells in HIV-1 transmission and pathogenesis, an effective vaccine to bring the HIV-1 pandemic under control must be effective at the level of the key target cells in both the genital and gastrointestinal mucosae.
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Okamura, Hiroshi, Eiji Yumoto, and Kazunori Okamoto. "Wound Healing of Canine Vocal Folds after Phonosurgery." Annals of Otology, Rhinology & Laryngology 96, no. 4 (July 1987): 425–28. http://dx.doi.org/10.1177/000348948709600415.

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To develop phonosurgical techniques, the authors investigated the healing mechanisms of wounds on the vocal folds of canine larynges, and devised a method to cover the raw surfaces of such wounds. To restore the normal physiologic properties of the vocal folds, the normal mucosa should be removed as little as possible in phonosurgery. When the mucosa of the vocal folds is extensively removed by surgical intervention and the raw surface cannot be covered with the local pedicle flap, it should be covered with a free mucosal flap. We found an activated human fibrinogen concentrate, which is a biologic tissue adhesive, to be suitable for adhering a free mucosal flap to the raw surface by a laryngomicrosurgical approach.
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Diaz, Patricia I., Zhihong Xie, Takanori Sobue, Angela Thompson, Basak Biyikoglu, Austin Ricker, Laertis Ikonomou, and Anna Dongari-Bagtzoglou. "Synergistic Interaction between Candida albicans and Commensal Oral Streptococci in a NovelIn VitroMucosal Model." Infection and Immunity 80, no. 2 (November 21, 2011): 620–32. http://dx.doi.org/10.1128/iai.05896-11.

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ABSTRACTCandida albicansis a commensal colonizer of the gastrointestinal tract of humans, where it coexists with highly diverse bacterial communities. It is not clear whether this interaction limits or promotes the potential ofC. albicansto become an opportunistic pathogen. Here we investigate the interaction betweenC. albicansand three species of streptococci from the viridans group, which are ubiquitous and abundant oral commensal bacteria. The ability ofC. albicansto form biofilms withStreptococcus oralis,Streptococcus sanguinis, orStreptococcus gordoniiwas investigated using flow cell devices that allow abiotic biofilm formation under salivary flow. In addition, we designed a novel flow cell system that allows mucosal biofilm formation under conditions that mimic the environment in the oral and esophageal mucosae. It was observed thatC. albicansand streptococci formed a synergistic partnership whereC. albicanspromoted the ability of streptococci to form biofilms on abiotic surfaces or on the surface of an oral mucosa analogue. The increased ability of streptococci to form biofilms in the presence ofC. albicanscould not be explained by a growth-stimulatory effect since the streptococci were unaffected in their growth in planktonic coculture withC. albicans. Conversely, the presence of streptococci increased the ability ofC. albicansto invade organotypic models of the oral and esophageal mucosae under conditions of salivary flow. Moreover, characterization of mucosal invasion by the biofilm microorganisms suggested that the esophageal mucosa is more permissive to invasion than the oral mucosa. In summary,C. albicansand commensal oral streptococci display a synergistic interaction with implications for the pathogenic potential ofC. albicansin the upper gastrointestinal tract.
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Dissertations / Theses on the topic "Mucosal surfaces"

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Tosh, F. Donald. "Adherence of Candida albicans to mucosal surfaces." Thesis, University of Glasgow, 1991. http://theses.gla.ac.uk/40982/.

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The research described in this thesis was aimed at the characterization of the Candida adhesin, and elucidation of the nature of the human epithelial cell receptor with which it combines. Previous data have shown that the fibrillar mannoprotein layer, produced when Candida albicans is grown in high concentrations of galactose, contains the proteinaceous adhesin. Different Candida species from leukoplakia patients were assayed for their ability to adhere to buccal cells. The results supported previous conclusions that there is a relationship between the ability of different Candida albicans strains to adhere to epithelial cells and their capacity for cell surface modification. Extracellular polymeric material (EPM) was isolated from culture supernates of C. albicans after growth in medium containing 500 mM galactose. When used to pretreat buccal epithelial cells, EPM inhibited adherence, which suggested that it contains an adhesin that binds to, and blocks epithelial cell receptors. Fractionation of EPM by affinity chromatography was performed. An index, the adhesion inhibition index (AII) was used to compare the various "lectin-like" components isolated from crude EPM. These studies indicated that use of different buccal cell donors gave different results, with the same C. albicans strain. Attempts to resolve EPM by SDS-polyacrylamide gel electrophonesis had previously proved unsuccessful. However here, success was achieved using the silver-stain technique. Chemical and enzymatic digestion of the EPM indicated that the protein portion , of the glycoprotein was more important than the carbohydrate at inhibiting adherence. N-Glycanase, papain, mild alkali treatment of EPM, followed by Synsorb-H-2 affinity adsorption chromatography, resulted in a purification of the yeast adhesin of more than 220 fold, relative to the crude EPM (on a protein weight basis). The nature of the epithelial cell receptor for C. albicans was investigated with potential receptor analogues such as sugars, lectins, monoclonal antibodies and saliva. The adhesion of C. albicans to the buccal cells of blood groups A and O, was found to be significant with respect to secretor status but not blood group. Caution should be shown in the interpretation of sugar inhibition tests. Nevertheless, N-acetyl-D- galactosamine was the most effective single sugar as an inhibitor of adhesion for buccal cell donors of blood group A; N-acetyl-D-galactosamine is the immunodominant blood group sugar for group A cells and the possibility exists that the blood group oligosaccharide on the buccal cell surface functions as the receptor for yeast adhesion. Further work would be needed to establish whether the purified adhesin had any therapeutic value in treating Candida infections.
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Frede, Annika. "Modulation of inflammatory responses at mucosal surfaces by nanoparticle-based siRNA delivery." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/modulation-of-inflammatory-responses-at-mucosal-surfaces-by-nanoparticlebased-sirna-delivery(188e5303-0b29-4d14-8635-7d1fcf448270).html.

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In this thesis nanoparticles consisting of a calcium phosphate core encapsulated by poly(lactic-co-glycolic) acid and polyethylenimine were developed for the delivery of siRNA in vivo. The nanoparticles were efficiently endocytosed by different cell types in vitro without exhibiting cytotoxic characteristics. Without possessing endogenous immune response activating properties, the nanoparticles had a highly preferable composition for the delivery of siRNA and subsequent gene knockdown. The delivery of siRNA with nanoparticles was tested in two different murine disease models: DSS-induced colitis as model for human IBD and a TH1-induced lung inflammation as model for COPD. In IBD and COPD chemokines and cytokines are predominant players in the progression of the inflammatory response. The local interference of cytokine signalling mediated by siRNA-loaded nanoparticles might therefore be a promising new therapeutic approach. In both murine models, the aim was to deliver siRNA directed against inflammation related cytokines by nanoparticles for the local treatment of mucosal inflammation. The local administration of nanoparticles loaded with siRNA to mice suffering from intestinal or lung inflammation led to significantly decreased target gene expression on mRNA as well as protein level in biopsies from the target tissues. Furthermore, reduced cytokine levels were accompanied by diminished inflammatory pathologies and augmented clinical signs of sickness. The results of this thesis indicate that a specific and local modulation of inflammatory responses by nanoparticle-based siRNA delivery is feasible and demonstrates a major therapeutic potential.
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O'Mahony, Rachel Mary. "Novel inhibitors of adhesin-receptor interactions involved in microbial infection at mucosal surfaces." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446253/.

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Microorganisms are becoming increasingly resistant to current antimicrobial agents and therefore new strategies and agents are being developed to combat infection. One strategy is to target and block the first step of microbial infection (adhesion of the microbe to the host tissue) by using molecules that mimic (or antibodies against) the microbial adhesin or its complementary host cell receptor. Plants have also been shown to provide natural sources of antimicrobial substances as well as inhibit microbial adhesion. One major problem in adhesion-inhibition studies has been the accurate quantification of adhesion. Most investigators have relied on manual counting while a few have used automated methods using image analysis software. The first aim of this study was therefore to compare the effectiveness of several current software packages, to develop the most accurate method of quantification and to use this method to test potential inhibitors of microbial adhesion. The organisms under investigation in this project were Candida albicans and Helicobacter pylori, both of which are becoming resistant to available antibiotic treatments. A new and accurate method of quantification was developed for assessing microbial adhesion using 'Metamorph' image analysis software. Aided by this system, several domain antibodies, carbohydrates and plant extracts were found to be successful inhibitors of C. albicans and H.pylori adhesion in vitro and therefore have the potential to form the basis of new and alternative therapies to treat infection caused by these microorganisms. Additionally, because it is not fully known why H. pylori preferentially colonises specific topographical regions of the human stomach, the second aim was to compare its adhesion to different topographical regions of the stomach, in an attempt to explain this phenomenon. No difference was found between the receptors present in the antrum or fundus of inflamed human stomachs. However, further investigations involving both inflamed and non-inflamed stomachs are warranted.
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Sid, Hicham [Verfasser]. "Host-pathogen interactions during mono- and multicausal infections of avian mucosal surfaces / Hicham Sid." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2016. http://d-nb.info/1123677514/34.

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Islam, Ayesha. "Interactions of human immunodeficiency virus type 1 with mucosal epithelial surfaces and Candida albicans." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/interactions-of-human-immunodeficiency-virus-type-1-with-mucosal-epithelial-surfaces-and-candida-albicans(c8f83c82-f3af-469e-9790-8626f4b96d0f).html.

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Despite the magnitude of the HIV pandemic, the events involved in the initial HIV-1 entry into the body are not yet fully understood. Although the principle mode of HIV-1 transmission is through mucosal surfaces, the oral epithelium appears to be less susceptible to HIV-1 infection than vaginal epithelium. In addition, infections with co-pathogens that elicit immune activation, such as Candida albicans, may also promote HIV-1 infection. The project objectives are to determine whether (i) HIV-1 is able to bind and integrate into oral and vaginal epithelial cell lines, (ii) epithelial cell lines are able to transfer viable virus from their surface to permissive cells, (iii) epithelial cells are responding to HIV-1 with changes in intracellular signalling or gene expression profiling, and (iv) Candida albicans can affect epithelial susceptibility to HIV-1 or whether it can bind and/or transfer HIV-1 to permissive cells. We demonstrate that oral, oro-pharyngeal and vaginal epithelial cell lines do not express canonical receptors for HIV-1 but they do express other receptors known to promote HIV-1 binding, including GalCer and syndecan-1. Oral and vaginal epithelial cell models can capture HIV-1, which subsequently does not appear to integrate into the epithelial genome. Therefore, viral replication is not supported. Notably, HIV-1 captured on the epithelial surface remains infectious and can be transferred to permissive cells. Furthermore, like epithelial cell lines, C. albicans can also directly bind and transfer HIV-1 to permissive cells. The carbohydrate moieties chitin and β-glucan appear to play a role in mediating viral binding. Notably, transfer of HIV-1 to permissive cells occurs from chitin but minimally from p-glucan. This indicates that fungal-viral interactions may occur at mucosal surfaces that potentially promote HIV-1 infection.
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Stange, Jörg. "Studies on host-pathogen interactions at mucosal barrier surfaces using the murine intestinal parasite Eimeria falciformis." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16716.

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Wir nutzten in dieser Studie den apikomplexen Parasiten Eimeria falciformis als Modell. Unsere Ergebnisse zeigen, dass das in infizierten Wildtypmäusen dominierende Zytokin IFN-γ für Immunschutz und für die Entwicklung der Darmpathologie entbehrlich war. E. falciformis-infizierte IFN-γR-/- and IFN-γ-/- Mäuse zeigten extremen Körpergewichtsverlust und starke Pathologie im Darm. Die Entwicklung des Parasiten in diesen Mäusen war überraschenderweise reduziert. Diese Beobachtungen gingen mit einer drastisch erhöhten Produktion von parasiten-spezifischem IL-17A und IL-22 durch CD4+ T Zellen einher. Gleichzeitige Neutralisierung von IL-17A und IL-22 in E. falciformis-infizierten IFN-γR-/- Mäusen verringerte den Körpergewichtsverlust und die Darmpathologie, und führte zu einer erhöhten Ausscheidung von Parasiten. Die Behandlung einer E. falciformis-infizierten intestinalen Epithelzelllinie mit IL-17A oder IL-22 führte zu einer signifikant reduzierten Entwicklung von E. falciformis in vitro. Diese Daten demonstrieren erstmalig einen anti-parasitären Effekt von IL-22 im Darm und deuten auf redundante Rollen von IL-17A und IL-22 im Hinblick auf die Förderung von Darmpathologie in Abwesenheit von IFN-γ hin. Um E. falciformis als Modellsystem weiter zu entwickeln, haben wir die Transfektion von E. falciformis Sporozoiten mit verschiedenen Plasmiden die den Reporter YFP und den Resistenzmarker DHTS enthalten etabliert. Rektal in Mäuse injizierte Sporozoiten entwickelten sich erfolgreich zu Oocysten, wenn auch mit geringerer Effizienz im Vergleich zur oralen Infektion mit Oozysten. Wiederholte in vivo Selektion YFP-exprimierender Oozysten führte zu Populationen mit maximal 34 % YFP-exprimierenden Parasiten. Wir demonstrieren in dieser Arbeit zum ersten Mal die Transfektion von E. falciformis und zeigen Perspektiven im Hinblick auf die Etablierung einer stabil transgenen Parasitenlinie auf.
The roles of Th1 and Th17 responses as mediators of host protection and pathology in the intestine are the subjects of intense research. Here we investigated a model of intestinal inflammation driven by the intracellular apicomplexan parasite Eimeria falciformis. Although IFN-γ was the predominant cytokine during E. falciformis infection in wild type mice, it was found to be dispensable for host defence and the development of infection-driven intestinal inflammation. E. falciformis-infected IFN-γR-/- and IFN-γ-/- mice developed dramatically exacerbated body weight loss and intestinal pathology, but surprisingly harboured fewer parasites. This was associated with a striking increase in parasite-specific IL-17A and IL-22 production in the mesenteric lymph nodes and at the site of infection. Concurrent neutralisation of IL-17A and IL-22 in E. falciformis infected IFN-γR-/- mice resulted in a reduction in infection induced body weight loss and inflammation and significantly increased parasite shedding. Taken together these data demonstrate for the first time an anti-parasitic effect of IL-22 during an intestinal infection and suggest that IL-17A and IL-22 have redundant roles in driving intestinal pathology in the absence of IFN-γ signalling. To further develop E. falciformis as a model system, we established transfection of E. falciformis sporozoites using various plasmids that contain the fluorescent reporter YFP and the resistance marker DHTS. Sporozoites applied rectally to mice were shown to complete their life cycle, albeit with a lower efficiency in comparison to oral infection with oocysts. Repeated in vivo selection using pyrimethamine and/or FACS and manual sorting led to a maximum percentage of 34 % YFP-expressing oocysts. Taken together, we demonstrate for the first time transfection of E. falciformis and provide perspectives for further work on the establishment of a stable transgenic parasite line.
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Shawky, Samia Ali. "Maternally acquired immunoglobulin G in turkey poults : distribution on mucosal surfaces and protective role in the gut /." The Ohio State University, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487842372894338.

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Clarke, Christopher John. "Antigen presentation to mucosal surfaces : the influence of liposome entrapment and cholera toxin on the immune response to fed protein antigens." Thesis, University of Bristol, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.330040.

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Stange, Jörg [Verfasser], Richard [Akademischer Betreuer] Lucius, Kai [Akademischer Betreuer] Matuschewski, and Alf [Akademischer Betreuer] Hamann. "Studies on host-pathogen interactions at mucosal barrier surfaces using the murine intestinal parasite Eimeria falciformis / Jörg Stange. Gutachter: Richard Lucius ; Kai Matuschewski ; Alf Hamann." Berlin : Humboldt Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://d-nb.info/1033837199/34.

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Burden, Matthew. "An investigation into making a bispecific scFv antibody that recognises both pIgR. and IgG Fc by phage display technology in order to transport IgG to mucosal surfaces." Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486114.

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The polymeric immunoglobulin receptor (pIgR) transports polymeric immunoglobulins across the epithelial cell layer into mucosal secretions. It was hoped that pIgR could be exploited to actively transport IgG by constructing a bispecific· molecule capable of simultaneously binding IgG and pIgR. Increasing the IgG' delivered to mucosal secretions may benefit patients undergoing intravenous immunoglobulin therapy by increasing the mucosal defence against invading pathogens. Phage display, using synthetic phagemid libraries (I and J), was used to generate scFv to secretory component (SC), the extracellular portion of pIgR. Phage raised against peptides of pIgR yielded no SC binding clones. Subsequent selections against SC were successful. An in vitro transport assay was used to measure transport of anti-SC clones. No transport could be detected in the initial assay, so it was optimised to increase sensitivity. Subsequent selections using this assay suggested that the dominant epitope recognised by the J library in SC was distinct from those that bound on pIgR that led to the highest level of transport. The dominant epitope recognised by the I library was present on both pIgR and SC. The clones were of weak binding possibly because of the restrictive design ofthe library and apparent bias seen in the sequences ofthe unselected clones. Affinity maturation was applied to the VL CDR3 in an attempt to improve the level of transcytosis of an anti-SC clone in the transport assay. A small improvement of transport was observed. Recombinant techniques used to create a bispecific scFv tandem were unsuocessful, in that its construction led to loss of binding specificities of both scFvs. Investigations in vivo were carried out as the first step of establishing an assay to test the final bispecific reagent. Study of the transport of an anti-pIgR phage suggested it was enriched compared to control phage in the faeces of mice injected intravenously.
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Books on the topic "Mucosal surfaces"

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Nataro, James P., Paul S. Cohen, Harry L. T. Mobley, and Jeffrey N. Weiser, eds. Colonization of Mucosal Surfaces. Washington, DC, USA: ASM Press, 2005. http://dx.doi.org/10.1128/9781555817619.

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Kraehenbuhl, Jean-Pierre, and Marian R. Neutra, eds. Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59951-4.

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Warren, Strober, ed. Mucosal immunity and infections at mucosal surfaces. New York: Oxford University Press, 1988.

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Colonization Of Mucosal Surfaces. ASM Press, 2005.

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Leceta, Javier, Rosa Del Campo, Stefan Jordan, and Christoph Siegfried Niki Klose, eds. Immunoregulation at Mucosal Surfaces. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-014-9.

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Nataro, James P., Paul S. Cohen, Harry L. T. Mobley, and Jeffrey N. Weiser. Colonization of Mucosal Surfaces. Wiley & Sons, Limited, John, 2014.

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Defense of mucosal surfaces: Pathogenesis, immunity and vaccines. Berlin: Springer, 1999.

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-P, Kraehenbuhl J., and Neutra M. R, eds. Defense of mucosal surfaces: Pathogenesis, immunity and vaccines. Berlin: Springer, 1999.

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Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines. Springer, 2011.

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Kraehenbuhl, Jean-Pierre, and Marian R. Neutra. Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines. Springer London, Limited, 2012.

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Book chapters on the topic "Mucosal surfaces"

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Pearson, Jeff P., and Iain A. Brownlee. "Structure and Function of Mucosal Surfaces." In Colonization of Mucosal Surfaces, 1–16. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch1.

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Dowson, Christopher G. "Genetic Exchange in the Respiratory Tract." In Colonization of Mucosal Surfaces, 131–40. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch10.

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Cotter, Peggy A. "Regulation in Response to Environmental Conditions." In Colonization of Mucosal Surfaces, 141–59. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch11.

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Tannock, Gerald W. "Microbiota of Mucosal Surfaces in the Gut of Monogastric Animals." In Colonization of Mucosal Surfaces, 161–78. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch12.

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Nataro, James P. "Interactions of the Commensal Flora with the Human Gastrointestinal Tract." In Colonization of Mucosal Surfaces, 179–86. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch13.

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Kaper, James B., Christopher Prichett, and Jane Michalski. "Quorum Sensing in the Gastrointestinal Tract." In Colonization of Mucosal Surfaces, 187–98. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch14.

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Laux, David C., Paul S. Cohen, and Tyrrell Conway. "Role of the Mucus Layer in Bacterial Colonization of the Intestine." In Colonization of Mucosal Surfaces, 199–212. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch15.

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Girón, Jorge A. "Role of Flagella in Mucosal Colonization." In Colonization of Mucosal Surfaces, 213–35. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch16.

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Hartland, Elizabeth L., Roy M. Robins-Browne, Alan D. Philips, and Gad Frankel. "Tissue Tropism in Intestinal Colonization." In Colonization of Mucosal Surfaces, 237–51. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch17.

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Nataro, James P., and Angela Jansen. "Aggregation and Dispersal on Mucosal Surfaces." In Colonization of Mucosal Surfaces, 253–63. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817619.ch18.

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Conference papers on the topic "Mucosal surfaces"

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DOUGAN, GORDON, MARJAN GHAEM-MAGHAMI, DEREK PICKARD, GAD FRANKEL, GILL DOUCE, SIMON CLARE, SARAH DUNSTAN, and CAMERON SIMMONS. "THE IMMUNE RESPONSES TO BACTERIAL ANTIGENS ENCOUNTERED IN VIVO AT MUCOSAL SURFACES." In The Activities of Bacterial Pathogens in Vivo - Based on Contributions to a Royal Society Discussion Meeting. IMPERIAL COLLEGE PRESS, 2001. http://dx.doi.org/10.1142/9781848161610_0014.

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Andersson, CK, M. Mori, AA Humbles, R. Kolbeck, AJ Coyle, CG Lofdahl, L. Bjermer, and JS Erjefalt. "Interleukin-33, a Novel “Alarmin” at Mucosal Surfaces, Is Up-Regulated in COPD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3791.

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Rutkowski, Melanie R., and Jose R. Conejo-Garcia. "Abstract IA32: Commensal microorganisms and polymorphic mucosal surfaces determine the evolution of distal metastatic tumors." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-ia32.

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Tzeng, Tzuen-Rong J., Yunyan R. Cheng, Reza Saeidpourazar, Siddharth Sanjeev Aphale, and Nader Jalili. "Adhesin-Specific Nanomechnical Cantilever Biosensors for Detection of Microorganisms." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18487.

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Considerable evidence has indicated that lectins (adhesins) on bacterial surfaces play an important role in the initiation of infection by mediating bacterial adherence to epithelial cell, especially in the gastrointestinal and urinary tracts. Many bacteria express adhesins on their surfaces in the form of specialized organelles that seek and bind to cognate receptors on the surface of mucosal cells. Some of these specific receptors have been reported and many of them are carbohydrates in nature. We have explored the use of specific carbohydrate receptors for the functionalization of nanoparticles and demonstrated their binding specificities and their ability to mediate aggregations of targeted bacteria. Based on these binding specificities, here we report the development of adhensin-specific nanomechanical cantilever (microcantilever) biosensors for the detection of their targeted microorganisms.
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Kanamori, Katsuhiro. "Image enhancement of surface micro-structure on mucosa for polarimetric endoscopy." In SPIE BiOS, edited by Robert R. Alfano and Stavros G. Demos. SPIE, 2015. http://dx.doi.org/10.1117/12.2075787.

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Krishnakumar, D., and K. S. Jaganathan. "Development of nasal HPV vaccine formulations." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685403.

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Cervical cancer is the second most cancer in women worldwide with over 500000 new cases and 275000 deaths being registered every year. With nearly 73000 women dying every year, India now tops the world in cervical cancer deaths. India represents 26.4% of all women dying of cervical cancer globally. Cervical cancer estimated to be responsible for about 5% of human cancers worldwide. Currently available vaccines may not provide complete protection against all HPV types as the protection is primarily type specific. Furthermore, the available vaccines are delivered via intramuscular route and require three doses and require cold chain supply which increases the cost of vaccine. Therefore a single dose vaccine delivered via non-invasive route (nasal) that protects against multiple HPV types would be a cost effective and better alternative to the currently available HPV vaccines. The main objective of this study was to prepare HPV antigen loaded poly (lactic-co-glycolic acid) (PLGA) and Tri Methyl Chitosan (TMC) coated PLGA microparticles and compare their efficacy as nasal vaccine. The developed formulations were characterized for size, zeta potential, entrapment efficiency, mucin adsorption ability, in vitro and in vivo studies. PLGA microparticles demonstrated negative zeta potential whereas PLGA-TMC microparticles showed higher positive zeta potential. The protein loading efficiency was found as above 80%. Results indicated that PLGA-TMC microparticles demonstrated substantially higher mucin adsorption when compared to PLGA microparticles. HPV antigen encapsulated in PLGA-TMC particles elicited a significantly higher secretory (IgA) immune response compared to that encapsulated in PLGA particles. Present study demonstrates that PLGA-TMC microparticles with specific size range can be a better carrier adjuvant for nasal subunit vaccines. Surface modified PLGA microparticles proved great potential as a nasal delivery system for HPV infections where systemic and mucosal responses are necessary particularly in conditions after viral pathogens invade the host through the mucosal surface.
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Melo, Arthur A., Eloise P. Rodrigues, Antonio M. N. Lima, Cleumar S. Moreira, and Rossana M. S. Cruz. "In Silico Study of the Surface Plasmon Resonance Use for Detecting Cancer in the Colorectal Mucosa." In 2022 IEEE International Instrumentation and Measurement Technology Conference (I2MTC). IEEE, 2022. http://dx.doi.org/10.1109/i2mtc48687.2022.9806452.

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Terry, Benjamin S., Jonathan A. Schoen, Allison B. Lyle, and Mark E. Rentschler. "Preliminary Mechanical Characterization of the Small Bowel for In Vivo Mobility." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-37010.

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In this work we present test methods, devices, and preliminary results for the mechanical characterization of the small bowel for intraluminal mobility. Both active and passive forces that affect mobility are investigated. The active forces are generated by the migrating motor complex and the movement of muscular organs within and surrounding the peritoneal cavity. Passive forces develop from the biomechanical response of the tissue, the tribology of the mucosa, mucoadhesion, and the orientation and mass of surrounding tissue. Four investigative devices and testing methods to characterize the active and passive forces are presented in this work. These are: 1) A novel manometer and a force sensor array that measure forces generated by the migrating motor complex; 2) A biaxial test apparatus and method for characterizing the biomechanical properties of the duodenum, jejunum, and ileum; 3) A novel in vitro protocol and device designed to measure the force required to overcome mucoadhesion; 4) A novel tribometer that measures in vivo coefficient of friction between the mucus membrane and the robot surface.
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Wurzinger, L. J., K. Herbst, and H. Schmid-Schonbein. "PLATELET AGGREGATE-ASSOCIATED FIBRIN FORMATION AS A FUNCTION OF AGGREGATE SIZE AND HEPARIN CONCENTRATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644857.

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The in vitro observation that fibrin forms withina few minutes in the crevices and niches inside and on the surface of platelet aggregates (PA), preparedfrom heparinized (5 U/ml) blood is consistent with the doubtful efficiency of heparin in the treatment of occlusive arterial disease (Thrcmb. Haemost. 46: 666,1981). Release of heparin- neutralizing proteins into limited and largely disclosed plasma compartments between aggregated platelets was held responsible for this remarkable phenomenon. However, the minimum number of aggregated platelets necessary to overcome the heparin inhibition remained undetermined then.PRP prepared from whole blood ant^coagulated with 0.5, 1 and 5 U/ml of mucosal heparin (Liquemin ), was aggregated with 10 or 100 pM ADP for 2 min at 37°C. Single PAs of various dimensions were withdrawn, washed, and incubated with a chromogenic substrate (S-2238, Kabi AB) to measure their thrombin content. Subsequently the number of platelets contained in the PA was evaluated by assaying the protein content of the aggregates. Microscopic PAs, their mass being toosmall to be determined precisely by a protein assay, were isolated with a filter technique, their extension was documented on photomicrographs for later calculation of aggregate volume and platelet content, before they were incubated with S-2238. Aggregates toosmall to develop detectable amidolytic activity, were checked microscopically for fibrin formed.S 2238 amidolytic activity (thrombin) in heparinizedPRP samples evolved as a linear function of the logarithm of PA mass. For a given heparin concentration (in whole blood) the following lowerthreshold platelet numbers of aggregates were found sufficient to allow the formation of detectable quantities of thrombin:These results suggest a fatal role platelet aggregates of minute dimensions may well play as a nidus of coagulation in fully heparinized blood.
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Consumi, Vanni, Lukas Lindenroth, Danail Stoyanov, and Agostino Stilli. "Design and experimental evaluation of the SOFTScreen Capsule System in a Colon Phantom." In The Hamlyn Symposium on Medical Robotics: "MedTech Reimagined". The Hamlyn Centre, Imperial College London London, UK, 2022. http://dx.doi.org/10.31256/hsmr2022.2.

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Colorectal cancer (CRC) is nowadays one of the deadliest cancer but the high surviving rate is achievable if the disease is diagnosticated and treated at the early stage. However, the standard procedure represents a discomfortable treatment for many patients at the point that many are discouraged in undergoing routine screening program. In fact, the clinician has to insert and guide by hand a semi-flexible tubular colonoscope and might apply significant forces and torques on the colon walls, with the complications of creating loops in the intestine, tissue damage or even perforation. For this reason, research in capsule robotic colonoscopy is in high demand [1]; the main objective of robotics in this field is to design a system capable of navigating inside the large intestine in order to provide visual inspection of the lumen, possibly, carrying surgical tools required in the colonoscopy procedure, i.e. polypectomy, without the creation of large pushing forces and loops. Human colon is about 130 cm long and composed by 4 consecutive tracts, joint at different angles, named sigmoid, descending, transverse and ascending colon. The diameter the tubular organ can changes from 25 mm to 70 mm, reaching up to 80 mm if insufflated with CO2 gas, often adopted in colonoscopy. Nonetheless, colon wall is a multilayers membrane that consists of four main layers (mucosa, submucosa, muscularis externa and serosa) which makes the membrane very compliant to large deformation and very slippery, being the internal wall of the colon characterized by continuous secretion of mucus Due to both the morphology and the frictional behaviour of the colon, the design of robots that are able to crawl the intestine and perform the screening of the organ is a challenge. Various locomotion strategies for micro robotic devices have been explored, such active capsules inspired by bio-mimetic locomotion strategies, such insect or caterpillar, or by use of locomoting members to self- propel once inside the colon such wheels or tracks [2]. Nonetheless, current robotic solutions are still far away to replace the standard colonoscopy due to the challenges in integrating reliable locomotion strategy in small size robots able to face the complex environment represented by the colon. In this work, we discuss the design and the features of the SOFTScreen system [3], discussing the testing of its locomotion capability inside a silicone phantom resembling the colon surface.
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