Elke Cario

ORCID: 0000-0003-2472-4495
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About
Contact & Profiles
Research Areas
  • Immune Response and Inflammation
  • Helicobacter pylori-related gastroenterology studies
  • Inflammatory Bowel Disease
  • IL-33, ST2, and ILC Pathways
  • Pediatric health and respiratory diseases
  • NF-κB Signaling Pathways
  • Immune Cell Function and Interaction
  • Drug Transport and Resistance Mechanisms
  • Gut microbiota and health
  • Microscopic Colitis
  • Mycobacterium research and diagnosis
  • Immunodeficiency and Autoimmune Disorders
  • Cancer Immunotherapy and Biomarkers
  • Escherichia coli research studies
  • Connexins and lens biology
  • Oral health in cancer treatment
  • Pediatric Hepatobiliary Diseases and Treatments
  • Neutropenia and Cancer Infections
  • Clinical Nutrition and Gastroenterology
  • Barrier Structure and Function Studies
  • Cytokine Signaling Pathways and Interactions
  • Viral gastroenteritis research and epidemiology
  • Pneumocystis jirovecii pneumonia detection and treatment
  • Infant Nutrition and Health
  • Immunotherapy and Immune Responses

University of Duisburg-Essen
2009-2020

Essen University Hospital
2007-2019

GTx (United States)
2016

Virginia Commonwealth University Medical Center
2011

Philadelphia University
2011

University of Aberdeen
2011

University of New Haven
2011

New York Proton Center
2011

Southwestern University
2011

University of Chicago
2011

ABSTRACT Initiation and perpetuation of the inflammatory intestinal responses in bowel disease (IBD) may result from an exaggerated host defense reaction epithelium to endogenous lumenal bacterial flora. Intestinal epithelial cell lines constitutively express several functional Toll-like receptors (TLRs) which appear be key regulators innate response system. The aim this study was characterize expression pattern TLR2, TLR3, TLR4, TLR5 primary cells patients with IBD. Small colonic biopsy...

10.1128/iai.68.12.7010-7017.2000 article EN Infection and Immunity 2000-12-01

Abstract LPS elicits several immediate proinflammatoy responses in peripheral blood leukocytes via a recently described pathway including CD14, Toll-like receptors (TLR), serine-threonine kinases, and NF-κB transcription factor. However, the functional of intestinal epithelial cells (IEC) to stimulation with are unknown. Expression mRNA protein for CD14 TLRs were assessed by RT-PCR, immunoblotting, immunohistochemistry mouse human IEC lines. LPS-induced activation signaling pathways (p42/p44...

10.4049/jimmunol.164.2.966 article EN The Journal of Immunology 2000-01-15

Gap junctional intercellular communication (GJIC) coordinates cellular functions essential for sustaining tissue homeostasis; yet its regulation in the intestine is not well understood. Here, we identify a novel physiological link between Toll-like receptor (TLR) 2 and GJIC through modulation of Connexin-43 (Cx43) during acute chronic inflammatory injury intestinal epithelial cell (IEC) barrier. Data from vitro studies reveal that TLR2 activation modulates Cx43 synthesis increases via IEC...

10.1074/jbc.m901619200 article EN cc-by Journal of Biological Chemistry 2009-06-16

Abstract Intestinal mucositis represents the most common complication of intensive chemotherapy, which has a severe adverse impact on quality life cancer patients. However, precise pathophysiology remains to be clarified, and there is so far no successful therapeutic intervention. In this study, we investigated role innate immunity through TLR signaling in modulating genotoxic chemotherapy-induced small intestinal injury vitro vivo. Genetic deletion TLR2, but not MD-2, mice resulted proximal...

10.4049/jimmunol.1402481 article EN The Journal of Immunology 2015-01-15

Mucinous adenocarcinoma (MAC) represents a distinct histopathological entity of colorectal cancer (CRC), which is associated with disease progression and poor prognosis. Here, we found that expression levels miR-205 miR-373 were specifically upregulated only in patients mucinous colon cancers, but not CRC lack components. To investigate the effects on intestinal epithelial cell (IEC) biology by gain- loss-of-function experiments proof-of-concept approach, chose previously established...

10.1371/journal.pone.0156871 article EN cc-by PLoS ONE 2016-06-06

DNA methylation is one of the major epigenetic mechanisms implicated in regulating cellular development and cell-type-specific gene expression. Here we performed simultaneous genome-wide expression analysis on purified intestinal epithelial cells derived from human fetal gut, healthy pediatric biopsies, children newly diagnosed with inflammatory bowel disease (IBD). Results were validated using pyrosequencing, real-time PCR, immunostaining. The functional impact changes was assessed by...

10.1038/mi.2015.88 article EN cc-by-nc-nd Mucosal Immunology 2015-09-16

Variants of the multidrug resistance gene (MDR1/ABCB1) have been associated with increased susceptibility to severe ulcerative colitis (UC). In this study, we investigated role TLR/IL-1R signaling pathways including common adaptor MyD88 in pathogenesis chronic colonic inflammation MDR1A deficiency. Double- or triple-null mice lacking TLR2, MD-2, MyD88, and were generated FVB/N background. Deletion TLR2 deficiency resulted fulminant pancolitis early expansion CD11b(+) myeloid cells rapid...

10.4049/jimmunol.1201592 article EN The Journal of Immunology 2013-05-02

Intestinal epithelial cells (IEC) are constantly exposed to both high concentrations of the bacterial ligand LPS and serine protease trypsin. MD-2, which contains multiple trypsin cleavage sites, is an essential accessory glycoprotein required for recognition signaling through TLR4. The aim this study was characterize expression subcellular distribution intestinal MD-2 delineate potential functional interactions with then alteration in inflammatory bowel disease (IBD). Although protein...

10.4049/jimmunol.176.7.4258 article EN The Journal of Immunology 2006-04-01

Epithelial cells of many mucosal organs have adapted to coexist with microbes and microbial products. In general, most studies suggest that epithelial benefit from interactions commensal microorganisms present at the lumenal surface. However, potentially injurious molecules found in this microenvironment also capacity elicit local inflammatory responses even systemic disease. We recently demonstrated epithelia express anti-infective molecule bactericidal/permeability-increasing protein...

10.1152/ajpgi.00347.2005 article EN AJP Gastrointestinal and Liver Physiology 2005-11-11
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