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        <title>Gut Pathogens - Most accessed articles</title>
        <link>http://www.gutpathogens.com</link>
        <description>The most accessed research articles published by Gut Pathogens</description>
        <dc:date>2012-04-25T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.gutpathogens.com/content/1/1/19" />
                                <rdf:li rdf:resource="http://www.gutpathogens.com/content/4/1/3" />
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                                <rdf:li rdf:resource="http://www.gutpathogens.com/content/1/1/15" />
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                                <rdf:li rdf:resource="http://www.gutpathogens.com/content/2/1/8" />
                                <rdf:li rdf:resource="http://www.gutpathogens.com/content/2/1/21" />
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        <item rdf:about="http://www.gutpathogens.com/content/3/1/1">
        <title>Acne vulgaris, probiotics and the gut-brain-skin axis - back to the future?</title>
        <description>Over 70 years have passed since dermatologists John H. Stokes and Donald M. Pillsbury first proposed a gastrointestinal mechanism for the overlap between depression, anxiety and skin conditions such as acne. Stokes and Pillsbury hypothesized that emotional states might alter the normal intestinal microflora, increase intestinal permeability and contribute to systemic inflammation. Among the remedies advocated by Stokes and Pillsbury were Lactobacillus acidophilus cultures. Many aspects of this gut-brain-skin unifying theory have recently been validated. The ability of the gut microbiota and oral probiotics to influence systemic inflammation, oxidative stress, glycemic control, tissue lipid content and even mood itself, may have important implications in acne. The intestinal microflora may also provide a twist to the developing diet and acne research. Here we provide a historical perspective to the contemporary investigations and clinical implications of the gut-brain-skin connection in acne.</description>
        <link>http://www.gutpathogens.com/content/3/1/1</link>
                <dc:creator>Whitney Bowe</dc:creator>
                <dc:creator>Alan Logan</dc:creator>
                <dc:source>Gut Pathogens 2011, null:1</dc:source>
        <dc:date>2011-01-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-3-1</dc:identifier>
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        <item rdf:about="http://www.gutpathogens.com/content/1/1/19">
        <title>Probiotics and gastrointestinal disease: successes, problems and future prospects</title>
        <description>Gastrointestinal disease is a major cause of morbidity and mortality worldwide each year. Treatment of chronic inflammatory gastrointestinal conditions such as ulcerative colitis and Crohn&apos;s disease is difficult due to the ambiguity surrounding their precise aetiology. Infectious gastrointestinal diseases, such as various types of diarrheal disease are also becoming increasingly difficult to treat due to the increasing dissemination of antibiotic resistance among microorganisms and the emergence of the so-called &apos;superbugs&apos;. Taking into consideration these problems, the need for novel therapeutics is essential. Although described for over a century probiotics have only been extensively researched in recent years. Their use in the treatment and prevention of disease, particularly gastrointestinal disease, has yielded many successful results, some of which we outline in this review. Although promising, many probiotics are hindered by inherent physiological and technological weaknesses and often the most clinically promising strains are unusable. Consequently we discuss various strategies whereby probiotics may be engineered to create designer probiotics. Such innovative approaches include; a receptor mimicry strategy to create probiotics that target specific pathogens and toxins, a patho-biotechnology approach using pathogen-derived genes to create more robust probiotic stains with increased host and processing-associated stress tolerance profiles and meta-biotechnology, whereby, functional metagenomics may be used to identify novel genes from diverse and vastly unexplored environments, such as the human gut, for use in biotechnology and medicine.</description>
        <link>http://www.gutpathogens.com/content/1/1/19</link>
                <dc:creator>Eamonn Culligan</dc:creator>
                <dc:creator>Colin Hill</dc:creator>
                <dc:creator>Roy Sleator</dc:creator>
                <dc:source>Gut Pathogens 2009, null:19</dc:source>
        <dc:date>2009-11-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-1-19</dc:identifier>
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        <prism:startingPage>19</prism:startingPage>
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        <item rdf:about="http://www.gutpathogens.com/content/4/1/3">
        <title>Rapid paracellular transmigration of Campylobacter
jejuni across polarized epithelial cells without
affecting TER: role of proteolytic-active HtrA
cleaving E-cadherin but not fibronectin</title>
        <description>Background:
Campylobacter jejuni is one of the most important bacterial pathogens causing food-borneillness worldwide. Crossing the intestinal epithelial barrier and host cell entry by C. jejuni isconsidered the primary reason of damage to the intestinal tissue, but the molecularmechanisms as well as major bacterial and host cell factors involved in this process are stillwidely unclear.
Results:
In the present study, we characterized the serine protease HtrA (high-temperaturerequirement A) of C. jejuni as a secreted virulence factor with important proteolyticfunctions. Infection studies and in vitro cleavage assays showed that C. jejuni&apos;s HtrA triggersshedding of the extracellular E-cadherin NTF domain (90 kDa) of non-polarised INT-407 andpolarized MKN-28 epithelial cells, but fibronectin was not cleaved as seen for H. pylori&apos;sHtrA. Deletion of the htrA gene in C. jejuni or expression of a protease-deficient S197A pointmutant did not lead to loss of flagella or reduced bacterial motility, but led to severe defectsin E-cadherin cleavage and transmigration of the bacteria across polarized MKN-28 celllayers. Unlike other highly invasive pathogens, transmigration across polarized cells by wildtypeC. jejuni is highly efficient and is achieved within a few minutes of infection.Interestingly, E-cadherin cleavage by C. jejuni occurs in a limited fashion and transmigrationrequired the intact flagella as well as HtrA protease activity, but does not reducetransepithelial electrical resistance (TER) as seen with Salmonella, Shigella, Listeria orNeisseria.
Conclusion:
These results suggest that HtrA-mediated E-cadherin cleavage is involved in rapid crossing ofthe epithelial barrier by C. jejuni via a very specific mechanism using the paracellular route toreach basolateral surfaces, but does not cleave the fibronectin receptor which is necessary forcell entry.</description>
        <link>http://www.gutpathogens.com/content/4/1/3</link>
                <dc:creator>Manja Boehm</dc:creator>
                <dc:creator>Benjamin Hoy</dc:creator>
                <dc:creator>Manfred Rohde</dc:creator>
                <dc:creator>Nicole Tegtmeyer</dc:creator>
                <dc:creator>Kristoffer Bæk</dc:creator>
                <dc:creator>Omar Oyarzabal</dc:creator>
                <dc:creator>Lone Brøndsted</dc:creator>
                <dc:creator>Silja Wessler</dc:creator>
                <dc:creator>Steffen Backert</dc:creator>
                <dc:source>Gut Pathogens 2012, null:3</dc:source>
        <dc:date>2012-04-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-4-3</dc:identifier>
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        <prism:startingPage>3</prism:startingPage>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/2">
        <title>Helicobacter pylori: a poor man&apos;s gut pathogen?</title>
        <description>Helicobacter pylori is one of the human pathogens with highest prevalence around the world; yet, its principal mode of transmission remains largely unknown. The role of H. pylori in gastric disease and cancer has not been established until the end of the 20th century. Since then, its epidemiology has been extensively studied, and an accruing body of literature suggests that not all humans are equally at risk of infection by this gut pathogen. Here, we briefly review the different epidemiological aspects of H. pylori infection with emphasis on those factors related to human poverty. The epidemiology of H. pylori infection is characterized by marked differences between developing and developed countries, notably among children. In addition, congruent lines of evidence point out to socioeconomic factors and living standards as main determinants of the age-dependent acquisition rate of H. pylori, and consequently its prevalence. These data are alarming in the light of the changing global climate and birth rate, which are expected to change the demography of our planet, putting more children at risk of H. pylori and its complications for years to come.</description>
        <link>http://www.gutpathogens.com/content/2/1/2</link>
                <dc:creator>Mohammed Mahdy Khalifa</dc:creator>
                <dc:creator>Radwa Sharaf</dc:creator>
                <dc:creator>Ramy Aziz</dc:creator>
                <dc:source>Gut Pathogens 2010, null:2</dc:source>
        <dc:date>2010-03-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-2</dc:identifier>
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                <prism:publicationName>Gut Pathogens</prism:publicationName>
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        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2010-03-31T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/1/1/15">
        <title>Mycobacterium avium subspecies paratuberculosis, Crohn&apos;s disease 
and the Doomsday Scenario
</title>
        <description>Johne&apos;s disease is chronic inflammation of the intestine caused by Mycobacterium avium subspecies paratuberculosis. Infection and disease are mainly in domestic livestock but can affect many species including primates. Johne&apos;s is a new disease which emerged at the turn of the 19th and 20th centuries and principally involved Europe and North America. It has since spread to former low incidence regions to become a global problem. Crohn&apos;s disease is a chronic inflammation of the intestine in humans which emerged in Europe and North America mid 20th century and increased to become a major healthcare problem. It has now spread to former low incidence regions. Infected animals shed Mycobacterium avium subspecies paratuberculosis in milk and into the environment. Human populations are widely exposed. Outcomes maybe influenced by microbial phenotype. Exposure to extracellular forms of these pathogens may confer some natural protection; exposure to intracellular forms which have passaged through milk macrophages or environmental protists may pose a greater threat to humans particularly individuals with an inherited or acquired susceptibility. Hot spots of human disease such as in Winnipeg which sits on rock at the junction of two rivers may result from local exposure to high levels of waterborne pathogens brought down from farmland. When appropriate methods are used most people with Crohn&apos;s disease are found to be infected. There are no data which demonstrate that these pathogens are harmless to humans. An overwhelming balance of probability and Public health risk favours the conclusion that Mycobacterium avium subspecies paratuberculosis is also pathogenic for people. A two tier co-operative pathogenic mechanism is proposed in Crohn&apos;s disease. Intracellular infection with the primary pathogen widely distributed throughout the gut causes an immune dysregulation and a specific chronic enteric neuropathy with loss of mucosal integrity. Segments of gross inflammatory disease result from the perturbed neuroimmune response to penetration into the gut wall of secondary pathogens from the lumen. These include both normal gut organisms and educated members of the enteric microbiome such as more aggressive E. coli. More new diseases may arise from failure to apply a range of remedial measures to this longstanding zoonotic problem.</description>
        <link>http://www.gutpathogens.com/content/1/1/15</link>
                <dc:creator>John Hermon-Taylor</dc:creator>
                <dc:source>Gut Pathogens 2009, null:15</dc:source>
        <dc:date>2009-07-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-1-15</dc:identifier>
                                <prism:require>/content/figures/1757-4749-1-15-toc.gif</prism:require>
                <prism:publicationName>Gut Pathogens</prism:publicationName>
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        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>15</prism:startingPage>
        <prism:publicationDate>2009-07-14T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.gutpathogens.com/content/4/1/1">
        <title>Health impact of probiotics - vision and opportunities</title>
        <description>Our understanding of the role of the microbiota in our gut and other sites in our body is rapidly emerging and could lead to many new and innovative approaches for health care. The promise of the potential role of probiotics for the prevention and treatment of enteric and other infections as an effective solution needs to be realized. The meeting report summarizes the insights and learning from a recent symposium, &quot;Health Impact of Probiotics - Vision and Opportunities&quot; conducted in Mumbai by the Yakult India Microbiota and Probiotic Science Foundation and P.D. Hinduja National Hospital, Mumbai. The symposium reflected its objective of unraveling the potential role of probiotics for health benefits through presentations and discussions. Experts clearly highlighted the role of probiotics in improving various aspects of health and in immune modulation. The report also captures the debate and discussions on the challenges that are likely to be encountered for the use of probiotics in the country.</description>
        <link>http://www.gutpathogens.com/content/4/1/1</link>
                <dc:creator>Neerja Hajela</dc:creator>
                <dc:creator>Gopinath Balakrish Nair</dc:creator>
                <dc:creator>Philip Abraham</dc:creator>
                <dc:creator>Nirmal Ganguly</dc:creator>
                <dc:source>Gut Pathogens 2012, null:1</dc:source>
        <dc:date>2012-03-12T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-4-1</dc:identifier>
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                <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2012-03-12T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.gutpathogens.com/content/3/1/8">
        <title> Intestinal microflora and body mass index during the first three years of life: an observational study.</title>
        <description>Background:
Recent research on obesity has demonstrated that the intestinal microflora can have an important influence on host energy balance. The aim of the study was to investigate the relationship between the intestinal microflora and the body mass index in the first 3 years of life.
Results:
In a prospective study, a faecal sample from 138 infants was taken at the age of 3, 26 and 52 weeks and cultured on selective media for 6 bacterial genera. Between the age of 1 and 3 years the Body Mass Index Standard Deviation Score (BMI SDS) of these children was determined. The association between the intestinal flora and BMI SDS was assessed for each bacterial genus. A positive correlation was found between the Bacteroides fragilis concentration and the BMI SDS at the age of 3 and 26 weeks. The Staphylococcus concentration showed a negative correlation with the BMI SDS at the age of 3 and 52 weeks. A low intestinal ratio of Staphylococcus/Bacteroides fragilis at the age of 3 weeks, corresponding to a low Staphylococcus and a high Bacteroides fragilis concentration, was associated with a higher BMI SDS during the first three years of life.
Conclusion:
High intestinal Bacteroides fragilis and low Staphylococcus concentrations in infants between the age of 3 weeks and 1 year were associated with a higher risk of obesity later in life. This study could provide new targets for a better and more effective modulation of the intestinal microflora in infants.</description>
        <link>http://www.gutpathogens.com/content/3/1/8</link>
                <dc:creator>Carl Vael</dc:creator>
                <dc:creator>Stijn Verhulst</dc:creator>
                <dc:creator>Vera Nelen</dc:creator>
                <dc:creator>Herman Goossens</dc:creator>
                <dc:creator>Kristine Desager</dc:creator>
                <dc:source>Gut Pathogens 2011, null:8</dc:source>
        <dc:date>2011-05-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-3-8</dc:identifier>
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                <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2011-05-23T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/8">
        <title>Enteropathogenic Escherichia coli, Samonella, Shigella  and Yersinia:
cellular aspects of host-bacteria interactions in enteric diseases
</title>
        <description>A successful infection of the human intestine by enteropathogenic bacteria depends on the ability of bacteria to attach and colonize the intestinal epithelium and, in some cases, to invade the host cell, survive intracellularly and disseminate from cell to cell. To accomplish these processes bacteria have evolved an arsenal of molecules that are mostly secreted by dedicated type III secretion systems, and that interact with the host, subverting normal cellular functions. Here we overview the most important molecular strategies developed by enteropathogenic Escherichia 
coli, Salmonella enterica, Shigella flexneri, and Yersinia enterocolitica to cause enteric infections. Despite having evolved different effectors, these four microorganisms share common host cellular targets.</description>
        <link>http://www.gutpathogens.com/content/2/1/8</link>
                <dc:creator>Roberta Reis</dc:creator>
                <dc:creator>Fabiana Horn</dc:creator>
                <dc:source>Gut Pathogens 2010, null:8</dc:source>
        <dc:date>2010-07-22T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-8</dc:identifier>
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                <prism:publicationName>Gut Pathogens</prism:publicationName>
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        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2010-07-22T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/21">
        <title>Ulcerative colitis and Crohn&apos;s disease: is Mycobacterium avium subspecies paratuberculosis the common villain?</title>
        <description>Mycobacterium avium, subspecies paratuberculosis (MAP) causes a chronic disease of the intestines in dairy cows and a wide range of other animals, including nonhuman primates, called Johne&apos;s (&quot;Yo-knee&apos;s&quot;) disease. MAP has been consistently identified by a variety of techniques in humans with Crohn&apos;s disease. The research investigating the presence of MAP in patients with Crohn&apos;s disease has often identified MAP in the &quot;negative&quot; ulcerative colitis controls as well, suggesting that ulcerative colitis is also caused by MAP. Like other infectious diseases, dose, route of infection, age, sex and genes influence whether an individual infected with MAP develops ulcerative colitis or Crohn&apos;s disease. The apparently opposite role of smoking, increasing the risk of Crohn&apos;s disease while decreasing the risk of ulcerative colitis, is explained by a more careful review of the literature that reveals smoking causes an increase in both diseases but switches the phenotype from ulcerative colitis to Crohn&apos;s disease. MAP as the sole etiologic agent of both ulcerative colitis and Crohn&apos;s disease explains their common epidemiology, geographic distribution and familial and sporadic clusters, providing a unified hypothesis for the prevention and cure of the no longer &quot;idiopathic&quot; inflammatory bowel diseases.</description>
        <link>http://www.gutpathogens.com/content/2/1/21</link>
                <dc:creator>Ellen Pierce</dc:creator>
                <dc:source>Gut Pathogens 2010, null:21</dc:source>
        <dc:date>2010-12-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-21</dc:identifier>
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                <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>21</prism:startingPage>
        <prism:publicationDate>2010-12-17T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/3/1/2">
        <title>Treating critically ill patients with probiotics: beneficial or dangerous?</title>
        <description>Probiotic bacteria are live microorganisms which confer to health benefits of the host. They help to maintain the integrity of the intestinal barrier function by modulating the mucosal and systemic immune response of the host. These bacteria have proven their beneficial effect in several conditions of ulcerative colitis. More recently probiotics/synbiotics have been included in the treatment of critically ill patients. However to date it remains uncertain whether probiotics/synbiotics are beneficial or even dangerous to the clinical outcome of this patient group. This article reviews the current evidence of the use of bacteria in critically ill patients in intensive care settings.</description>
        <link>http://www.gutpathogens.com/content/3/1/2</link>
                <dc:creator>Christoph Jacobi</dc:creator>
                <dc:creator>Christian Schulz</dc:creator>
                <dc:creator>Peter Malfertheiner</dc:creator>
                <dc:source>Gut Pathogens 2011, null:2</dc:source>
        <dc:date>2011-02-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-3-2</dc:identifier>
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        <prism:startingPage>2</prism:startingPage>
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