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Find video protocols related to scientific articles indexed in Pubmed.
Candida albicans colonization and dissemination from the murine gastrointestinal tract: the influence of morphology and Th17 immunity.
Cell. Microbiol.
PUBLISHED: 10-21-2014
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The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonisation and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild type and morphological mutants of C. albicans in an established model of GI tract colonization, induced following antibiotic-treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C.?albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C. albicans, and have implications for our understanding of human disease.
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Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.
PLoS Pathog.
PUBLISHED: 04-01-2014
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Chitin is an essential structural polysaccharide of fungal pathogens and parasites, but its role in human immune responses remains largely unknown. It is the second most abundant polysaccharide in nature after cellulose and its derivatives today are widely used for medical and industrial purposes. We analysed the immunological properties of purified chitin particles derived from the opportunistic human fungal pathogen Candida albicans, which led to the selective secretion of the anti-inflammatory cytokine IL-10. We identified NOD2, TLR9 and the mannose receptor as essential fungal chitin-recognition receptors for the induction of this response. Chitin reduced LPS-induced inflammation in vivo and may therefore contribute to the resolution of the immune response once the pathogen has been defeated. Fungal chitin also induced eosinophilia in vivo, underpinning its ability to induce asthma. Polymorphisms in the identified chitin receptors, NOD2 and TLR9, predispose individuals to inflammatory conditions and dysregulated expression of chitinases and chitinase-like binding proteins, whose activity is essential to generate IL-10-inducing fungal chitin particles in vitro, have also been linked to inflammatory conditions and asthma. Chitin recognition is therefore critical for immune homeostasis and is likely to have a significant role in infectious and allergic disease.
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Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.
PLoS Pathog.
PUBLISHED: 04-01-2013
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The ?-glucan receptor Dectin-1 is a member of the C-type lectin family and functions as an innate pattern recognition receptor in antifungal immunity. In both mouse and man, Dectin-1 has been found to play an essential role in controlling infections with Candida albicans, a normally commensal fungus in man which can cause superficial mucocutaneous infections as well as life-threatening invasive diseases. Here, using in vivo models of infection, we show that the requirement for Dectin-1 in the control of systemic Candida albicans infections is fungal strain-specific; a phenotype that only becomes apparent during infection and cannot be recapitulated in vitro. Transcript analysis revealed that this differential requirement for Dectin-1 is due to variable adaptation of C. albicans strains in vivo, and that this results in substantial differences in the composition and nature of their cell walls. In particular, we established that differences in the levels of cell-wall chitin influence the role of Dectin-1, and that these effects can be modulated by antifungal drug treatment. Our results therefore provide substantial new insights into the interaction between C. albicans and the immune system and have significant implications for our understanding of susceptibility and treatment of human infections with this pathogen.
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C-type lectin receptors and cytokines in fungal immunity.
Cytokine
PUBLISHED: 08-05-2011
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Fungi are the cause of opportunistic infections, predominantly in immunocompromised individuals although, primary fungal infections can occur in apparently healthy individuals. Successful host defence requires an effective innate and adaptive immune response. Central to host immune responses are the induction of cytokines; the signals which help to activate the innate immune system and which play a central role in directing the development of pathogen-specific immunity. C-type lectins play a central role in the recognition and shaping of immune responses to fungal pathogens, in part, through the induction and modulation of cytokine responses. Understanding which cytokines induce protective responses to these pathogens and how C-type lectins and other receptors direct cytokine production may allow development of novel antifungal therapies. Here we review the C-type lectins, their influence on cytokine production and subsequent immune responses in antifungal immunity.
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C-type lectins, fungi and Th17 responses.
Cytokine Growth Factor Rev.
PUBLISHED: 11-12-2010
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Th17 cells are a recently discovered subset of T helper cells characterised by the release of IL-17, and are thought to be important for mobilization of immune responses against microbial pathogens, but which also contribute to the development of autoimmune diseases. The identification of C-type lectin receptors which are capable of regulating the balance between Th1 and Th17 responses has been of particular recent interest, which they control, in part, though the release of Th17 inducing cytokines. Many of these receptors recognise fungi, and other pathogens, and play key roles in driving the development of protective anti-microbial immunity. Here we will review the C-type lectins that have been linked to Th17 type responses and will briefly examine the role of Th17 responses in murine and human anti-fungal immunity.
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Dectin-1 is not required for controlling Candida albicans colonization of the gastrointestinal tract.
Infect. Immun.
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Candida albicans is normally found as a commensal microbe, commonly colonizing the gastrointestinal tract in humans. However, this fungus can also cause mucosal and systemic infections once immune function is compromised. Dectin-1 is an innate pattern recognition receptor essential for the control of fungal infections in both mice and humans; however, its role in the control of C. albicans colonization of the gastrointestinal tract has not been defined. Here, we demonstrate that in mice dectin-1 is essential for the control of gastrointestinal invasion during systemic infection, with dectin-1 deficiency associating with impaired fungal clearance and dysregulated cytokine production. Surprisingly, however, following oral infection, dectin-1 was not required for the control of mucosal colonization of the gastrointestinal tract, in terms of either fungal burdens or cytokine response. Thus, in mice, dectin-1 is essential for controlling systemic infection with C. albicans but appears to be redundant for the control of gastrointestinal colonization.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.