Publications by authors named "Zeli Shen"

Three strains were cultured from the eyes of CD36-knockout mice (B6.129S1-/J) with and without keratitis housed at a biomedical research institute. Bacteria were sequenced using Illumina MiSeq technology for subsequent phylogenetic characterization and identification of virulence factor genes conferring pathogenic potential.

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infects half of the world population and is the leading cause of gastric cancer. We previously demonstrated that gastric cancer risk is associated with gastric microbiota. Specifically, gastric urease-positive and had contrasting effects on -associated gastric pathology and immune responses in germ-free INS-GAS mice.

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spp., including the well-known human gastric pathogen , can cause gastric diseases in humans and other mammals. They are Gram-negative bacteria that colonize the gastric epithelium and use their multiple flagella to move across the protective gastric mucus layer.

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Along with infection, the gastric microbiota is hypothesized to modulate stomach cancer risk in susceptible individuals. Whole metagenomic shotgun sequencing (WMS) is a sequencing approach to characterize the microbiome with advantages over traditional culture and 16S rRNA sequencing including identification of bacterial and non-bacterial taxa, species/strain resolution, and functional characterization of the microbiota. In this study, we used WMS to survey the microbiome in extracted DNA from antral gastric biopsy samples from Colombian patients residing in the high-risk gastric cancer town Túquerres ( = 10, -positive = 7) and low-risk town of Tumaco ( = 10, -positive = 6).

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The loss of IL-10R function leads to severe early onset colitis and, in murine models, is associated with the accumulation of immature inflammatory colonic macrophages. We have shown that IL-10R-deficient colonic macrophages exhibit increased STAT1-dependent gene expression, suggesting that IL-10R-mediated inhibition of STAT1 signaling in newly recruited colonic macrophages might interfere with the development of an inflammatory phenotype. Indeed, STAT1 mice exhibit defects in colonic macrophage accumulation after Helicobacter hepaticus infection and IL-10R blockade, and this was phenocopied in mice lacking IFNγR, an inducer of STAT1 activation.

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Iron deficiency, the most common micronutrient deficiency in humans, is associated with long-term deficits in cognition and memory if left untreated. Infection with the gastric pathogen Helicobacter pylori has been linked to iron deficiency anemia (IDA). The H.

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Microbial colonization of the mammalian intestine elicits inflammatory or tolerogenic T cell responses, but the mechanisms controlling these distinct outcomes remain poorly understood, and accumulating evidence indicates that aberrant immunity to intestinal microbiota is causally associated with infectious, inflammatory and malignant diseases. Here we define a critical pathway controlling the fate of inflammatory versus tolerogenic T cells that respond to the microbiota and express the transcription factor RORγt. We profiled all RORγt immune cells at single-cell resolution from the intestine-draining lymph nodes of mice and reveal a dominant presence of T regulatory (T) cells and lymphoid tissue inducer-like group 3 innate lymphoid cells (ILC3s), which co-localize at interfollicular regions.

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In populations with similar prevalence of Helicobacter pylori infection, cancer risk can vary dramatically. Changes in composition or structure of bacterial communities in the stomach, either at the time of exposure or over the course of H. pylori infection, may contribute to gastric pathology.

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Escherichia coli strains encoding colibactin (pks), hemolysin-associated cytotoxic necrotizing factor (cnf), and cytolethal distending toxin (cdt) are associated with intestinal inflammation and cancer, urinary tract infection, and septicemia in susceptible hosts. Over a 2-year period, an inbred laboratory colony of specific-pathogen free (SPF) cats (∼25) presented with resorptions, stillbirths, and pyometras in >50 % of pregnancies. Hemolytic E.

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Background: The gut microbiome is altered in patients with inflammatory bowel disease, yet how these alterations contribute to intestinal inflammation is poorly understood. Murine models have demonstrated the importance of the microbiome in colitis since colitis fails to develop in many genetically susceptible animal models when re-derived into germ-free environments. We have previously shown that Wiskott-Aldrich syndrome protein (WASP)-deficient mice (Was) develop spontaneous colitis, similar to human patients with loss-of-function mutations in WAS.

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Both genetic predisposition and environmental factors appear to play a role in inflammatory bowel disease (IBD) development. Genetic studies in humans have linked the interleukin (IL)-23 signaling pathway with IBD, but the environmental factors contributing to disease have remained elusive. Here, we show that the azo dyes Red 40 and Yellow 6, the most abundant food colorants in the world, can trigger an IBD-like colitis in mice conditionally expressing IL-23, or in two additional animal models in which IL-23 expression was augmented.

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Colombia, South America has one of the world's highest burdens of infection and gastric cancer. While multidrug antibiotic regimens can effectively eradicate , treatment efficacy is being jeopardized by the emergence of antibiotic-resistant strains. Moreover, the spectrum of and genetic mechanisms for antibiotic resistance in Colombia is underreported.

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Article Synopsis
  • - The Blue Iguana Recovery Programme is focused on breeding and supporting the endangered Grand Cayman blue iguana, during which a novel bacteria named Helicobacter sp. GCBI1 was discovered in lethargic wild iguanas.
  • - Between 2015 and 2017, this bacteria was identified in 11 blue iguanas, resulting in two deaths and treatment for nine others, with only five surviving.
  • - Research indicates that the Grand Cayman blue iguanas do not carry or shed this bacteria asymptomatically, but green iguanas in the same region may be carriers; the source and transmission route for the infection are still not understood.
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( type 1) commonly infects nonhuman primates but its clinical importance is in question. To characterize infection in a colony of rhesus macaques () used in cognitive neuroscience research. Inquiries into the nature of in nonhuman primates are required to further define the organism's virulence and the experimental animal's gastric microbiome.

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Zebra finches (Taeniopygia guttata) are laboratory animal species commonly used for modeling neurobiology and learning. Historically, using bacterial culture, biochemical analysis, and 16S ribosomal RNA gene sequencing, bacterial isolates from feces of finches housed at Massachusetts Institute of Technology had been presumptively diagnosed as Campylobacter jejuni, which is commonly isolated from both domestic and wild birds. Although the zebra finches were not clinically affected, C.

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In a search for potential causes of increased prolapse incidence in grey short-tailed opossum colonies, samples from the gastrointestinal tracts of 94 clinically normal opossums with rectal prolapses were screened for species by culture and PCR. Forty strains of two novel species which differed from the established taxa were isolated from opossums with and without prolapses. One of the species was spiral-shaped and urease-negative whereas the other strain had fusiform morphology with periplasmic fibres and was urease-positive.

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species are being increasingly isolated and associated with disease in humans and animals. Here, we describe four draft genome sequences of species from nonhuman primates. These include , isolated from wild chimpanzees, and two likely new species isolated from a lemur, common marmoset, and cotton-top tamarin.

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Cotton-top tamarins (CTTs) are an ideal model of human inflammatory bowel disease (IBD) because these animals develop multigenerational, lower bowel cancer. We previously isolated and characterized a novel enterohepatic species, , from CTTs with IBD and documented that infection in germfree C57BL IL-10 mice recapitulates IBD, suggesting that influences IBD etiopathogenesis. In this study, we utilized a germfree IL-10 model to illustrate that infection can naturally transmit and infect four generations and cause significant intestinal inflammatory pathology.

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A fast-growing species was cultured from draining, purulent lesions on the caudal abdomen of a 12-year-old male domestic long-haired cat. Whole-genome sequencing identified the organism as .

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Mice deficient in the IL-10 pathway are the most widely used models of intestinal immunopathology. IL-17A is strongly implicated in gut disease in mice and humans, but conflicting evidence has drawn IL-17's role in the gut into question. IL-22 regulates antimicrobial and repair activities of intestinal epithelial cells (IECs) and is closely associated with IL-17A responses but it's role in chronic disease is uncertain.

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Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identified opposing effects on ILCs by two species, and , isolated from immunocompromised mice.

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Current methods for detecting mites in mouse colonies have limitations in terms of cost, accuracy, and throughput. To address these limitations, we developed PCR assays to detect in fecal samples. Using a newly generated ribosomal RNA sequence of (MC28S), we developed PCR and qPCR assays capable of detecting mites or eggs ingested during grooming.

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Background: The aim of this study was to longitudinally investigate the prevalence and characterization of Campylobacter spp. from non-human primates primate (NHP) with a history of endemic diarrhea housed at Como Park Zoo.

Methods: Fecal samples from 33 symptom-free NHP belonging to eight different species were collected weekly for 9 weeks.

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Background: The genus Helicobacter are gram-negative, microaerobic, flagellated, mucus-inhabiting bacteria associated with gastrointestinal inflammation and classified as gastric or enterohepatic Helicobacter species (EHS) according to host species and colonization niche. While there are over 30 official species, little is known about the physiology and pathogenic mechanisms of EHS, which account for most in the genus, as well as what genetic factors differentiate gastric versus EHS, given they inhabit different hosts and colonization niches. The objective of this study was to perform a whole-genus comparative analysis of over 100 gastric versus EHS genomes in order to identify genetic determinants that distinguish these Helicobacter species and provide insights about their evolution/adaptation to different hosts, colonization niches, and mechanisms of virulence.

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Background: Helicobacter saguini is a novel enterohepatic Helicobacter species isolated from captive cotton top tamarins with chronic colitis and colon cancer. Monoassociated H. saguini infection in gnotobiotic IL-10 mice causes typhlocolitis and dysplasia; however, the virulent mechanisms of this species are unknown.

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