Elizabeth Brint

ORCID: 0000-0001-9214-149X
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About
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Research Areas
  • Immune Response and Inflammation
  • IL-33, ST2, and ILC Pathways
  • NF-κB Signaling Pathways
  • Immune Cell Function and Interaction
  • Cancer Immunotherapy and Biomarkers
  • Psoriasis: Treatment and Pathogenesis
  • Inflammasome and immune disorders
  • Inflammatory Bowel Disease
  • Gastrointestinal motility and disorders
  • Helicobacter pylori-related gastroenterology studies
  • Cytokine Signaling Pathways and Interactions
  • interferon and immune responses
  • Eosinophilic Esophagitis
  • Microbial Inactivation Methods
  • Influenza Virus Research Studies
  • Toxin Mechanisms and Immunotoxins
  • Microfluidic and Bio-sensing Technologies
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Dermatology and Skin Diseases
  • Cell death mechanisms and regulation
  • Microscopic Colitis
  • Gut microbiota and health
  • Cancer Research and Treatments
  • Inflammatory mediators and NSAID effects
  • Immunotherapy and Immune Responses

University College Cork
2013-2025

Cork University Hospital
2010-2025

APC Microbiome Institute
2016-2023

National University of Ireland
2010-2016

Trinity College Dublin
2001-2006

In this study we have identified members of the Toll-like receptor (TLR) family (namely, TLRs 4, 6, 8, and 9) as proteins to which intracellular protein tyrosine kinase, Bruton's kinase (Btk), binds. Detailed analysis interaction between Btk TLR8 demonstrates that presence both Box 2 3 motifs in Toll/interleukin-1 domain was required for interaction. Furthermore, co-immunoprecipitation experiments revealed can also interact with key involved TLR4 signal transduction, namely, MyD88, Mal...

10.1074/jbc.m301484200 article EN cc-by Journal of Biological Chemistry 2003-07-01

OBJECTIVES: The pathogenesis of irritable bowel syndrome (IBS) is poorly understood. One contributory factor may be low-grade mucosal inflammation, perhaps initiated by the microbiota. Toll-like receptors (TLRs) are a family pathogen-recognition innate immune system. aim this study was to evaluate potential involvement TLRs in IBS further understand system complex disorder. METHODS: expression investigated colonic biopsy samples obtained from 26 patients and compared with 19 healthy...

10.1038/ajg.2010.438 article EN The American Journal of Gastroenterology 2010-11-23

Listeria monocytogenes is a Gram-positive bacterium that can cause septicemia and meningitis. TLRs are central receptors of the innate immune system drive inflammatory responses to invading microbes such as L. monocytogenes. Although intestinal epithelial cells (IECs) represent initial point entry used by for infection, response in these has been poorly characterized date. The aim this study was determine which involved mediating IECs. We performed an RNA interference screen 1-10 HT-29 IEC...

10.4049/jimmunol.1203245 article EN The Journal of Immunology 2013-11-07

PKCε has been shown to play a key role in the effect of Gram-negative bacterial product LPS; however, target for LPS signaling is unknown. mediated by Toll-like receptor 4, which uses four adapter proteins, MyD88, MyD88 adapter-like (Mal), Toll/IL-1R domain-containing inducing IFN-β (Trif), and Trif-related molecule (TRAM). Here we show that TRAM transiently phosphorylated on serine-16 an LPS-dependent manner. Activation IFN regulatory factor 3 induction chemokine RANTES, are both...

10.1073/pnas.0600462103 article EN Proceedings of the National Academy of Sciences 2006-06-07

Despite the importance of inflammation in cancer, role cytokine IL-33, and its receptor ST2, colon cancer is unclear. The aim this study was to investigate isoforms (ST2 ST2L), cancer. Serum levels IL-33 sST2 were determined with ELISA. ST2 expression detected quantitative real-time PCR (qRT–PCR), western blotting immunohistochemistry. CT26 cells stably suppressed using ST2-specific shRNA. Cytokine chemokine gene qRT–PCR. Human tumours showed lower ST2L as compared adjacent non-tumour tissue...

10.1038/bjc.2015.433 article EN cc-by-nc-sa British Journal of Cancer 2015-12-17

The Toll-interleukin-1 receptor domain-containing adapter Mal (MyD88 adapter-like protein) is involved in Toll-like (TLR)-2 and TLR4 signal transduction. However, no studies have yet identified a function for distinct from the related MyD88. In this study, we putative TRAF6 interaction site but not MyD88 demonstrate that can be co-immunoprecipitated with TRAF6. Overexpression of MalE190A, which contains mutation within TRAF6-binding motif, failed to induce expression an NF-kappaB-dependent...

10.1074/jbc.c400289200 article EN cc-by Journal of Biological Chemistry 2004-07-10

The innate immune system is currently seen as the probable initiator of events which culminate in development inflammatory bowel disease (IBD) with Toll-like receptors (TLRs) known to be involved this process. Many regulators TLRs have been described, and dysregulation these may also important pathogenesis IBD. aim study was perform a co-ordinated analysis expression levels both key intestinal their inhibitory proteins same IBD cohorts, ulcerative colitis (UC) Crohn's (CD), order evaluate...

10.1111/cei.12732 article EN cc-by-nc Clinical & Experimental Immunology 2015-10-14

This study found that patients with active UC have significantly increased colonic gene expression of cytosolic DNA sensor, inflammasome, STING, and type I IFN signaling pathways. The IFN, IFN-β, in combination TNF-α induced JAK-dependent but NLRP3 inflammasome-independent inflammatory cell death organoids. novel phenotype is relevant to immunopathology may partially explain the efficacy JAKinibs tofacitinib upadacitinib UC.

10.1152/ajpgi.00104.2022 article EN AJP Gastrointestinal and Liver Physiology 2022-09-27

T1/ST2 is a member of the interleukin (IL)-1 receptor superfamily, possessing three immunoglobulin domains extracellularly and Toll/IL1R (TIR) domain intracellularly. The ligand for not known. expressed on Type 2 T helper (Th2) cells, its role appears to be in regulation Th2 cell function. Here, we have investigated signal transduction, using either transient overexpression or cross-linking monoclonal antibody activate cells. We demonstrate that does transcription factor NF-κB when...

10.1074/jbc.m209685200 article EN cc-by Journal of Biological Chemistry 2002-12-01

Irritable bowel syndrome (IBS) is largely viewed as a stress-related disorder caused by aberrant brain-gut-immune communication and altered gastrointestinal (GI) homeostasis. Accumulating evidence demonstrates that stress modulates innate immune responses; however, very little known on the immunological effects of GI tract. Toll-like receptors (TLRs) are critical pattern recognition molecules system. Activation TLRs bacterial viral leads to activation NF-kB an increase in inflammatory...

10.1371/journal.pone.0008226 article EN cc-by PLoS ONE 2009-12-09

The IL-36 cytokines are a recently described subset of the IL-1 family cytokines, shown to play role in pathogenesis intestinal diseases such as Inflammatory Bowel Disease (IBD). Given link between IBD and colitis -associated cancer, well involvement other members tumorigenesis, aim this work was investigate whether colon cancer. Whilst research date has focused on augmenting immune response induce tumour rejection, very little remains known about IL-36R signalling cells context. In study we...

10.1038/s41388-022-02281-2 article EN cc-by Oncogene 2022-04-01

Bcl-3 is a member of the IκB family proteins and an essential negative regulator Toll-like receptor-induced responses. Recently, single nucleotide polymorphism associated with reduced gene expression has been identified as potential risk factor for Crohn's disease. Here we report that in contrast to predictions (SNP) analysis, patients disease ulcerative colitis demonstrate elevated mRNA relative healthy individuals. To explore further role inflammatory bowel (IBD), used dextran-sodium...

10.1111/cei.12119 article EN Clinical & Experimental Immunology 2013-04-15
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