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Pattern Recognition Receptors in Gastrointestinal Inflammation and Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (25 February 2023) | Viewed by 2361

Special Issue Editors

Department of Pathology, UT Southwestern Medical Center, Dallas, TX 75390, USA
Interests: cell signaling; diet and metabolic disorders; gastrointestinal inflammation and cancer; gut microbiome; host–pathogen interaction; NOD-like receptors
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Guest Editor
Department of Biology, Missouri State University, Springfield, MO 65897, USA
Interests: anti-inflammatory therapy; cell signaling; host–pathogen interaction; immunopathology; infectious disease; NOD-like receptors

Special Issue Information

Dear Colleagues,

The host immune system is equipped with various pattern recognition receptors (PRRs), which sense pathogen- or danger-associated molecular patterns at the cell surface or inside the cell. PPRs, including toll-like receptors (TLRs), NOD-like receptors (NLRs), retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), and nucleic acid sensors, play critical roles in host defense against infections and inflammatory disorders. Genetic and experimental studies have linked gastrointestinal disorders, such as inflammatory bowel diseases, colorectal cancer, and liver diseases, to dysfunction in several PRRs. It appears that TLRs, NLRs, and other PRRs provide protection against these diseases through the regulation of various cell signaling pathways, immune responses, physiological functions, and gut microbiota composition. This Special Issue aims to collect original research and review articles representing recent advances on the role of different PRRs in colitis, colorectal cancer, and other gastrointestinal disorders.

Dr. Hasan Zaki
Dr. Christopher Lupfer
Guest Editors

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Keywords

  • pattern recognition receptors
  • toll-like receptors (TLRs)
  • NOD-like receptors (NLRs)
  • RIG-I-like receptors
  • AIM2
  • DNA sensors
  • colitis
  • colorectal cancer
  • gastrointestinal inflammation
  • inflammatory bowel diseases
  • gut microbiota
  • host–pathogen interaction
  • inflammatory disorders
  • hepatocellular carcinoma
  • fatty liver syndrome
  • immunopathology

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Published Papers (1 paper)

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Research

17 pages, 2261 KiB  
Article
The Local Activation of Toll-like Receptor 7 (TLR7) Modulates Colonic Epithelial Barrier Function in Rats
by Javier Estévez and Vicente Martínez
Int. J. Mol. Sci. 2023, 24(2), 1254; https://doi.org/10.3390/ijms24021254 - 9 Jan 2023
Cited by 2 | Viewed by 2029
Abstract
Toll-like receptors (TLRs)-mediated host–bacterial interactions participate in the microbial regulation of gastrointestinal functions, including the epithelial barrier function (EBF). We evaluated the effects of TLR7 stimulation on the colonic EBF in rats. TLR7 was stimulated with the selective agonist imiquimod (100/300 µg/rat, intracolonic), [...] Read more.
Toll-like receptors (TLRs)-mediated host–bacterial interactions participate in the microbial regulation of gastrointestinal functions, including the epithelial barrier function (EBF). We evaluated the effects of TLR7 stimulation on the colonic EBF in rats. TLR7 was stimulated with the selective agonist imiquimod (100/300 µg/rat, intracolonic), with or without the intracolonic administration of dimethyl sulfoxide (DMSO). Colonic EBF was assessed in vitro (electrophysiology and permeability to macromolecules, Ussing chamber) and in vivo (passage of macromolecules to blood and urine). Changes in the expression (RT-qPCR) and distribution (immunohistochemistry) of tight junction-related proteins were determined. Expression of proglucagon, precursor of the barrier-enhancer factor glucagon-like peptide 2 (GLP-2) was also assessed (RT-qPCR). Intracolonic imiquimod enhanced the EBF in vitro, reducing the epithelial conductance and the passage of macromolecules, thus indicating a pro-barrier effect of TLR7. However, the combination of TLR7 stimulation and DMSO had a detrimental effect on the EBF, which manifested as an increased passage of macromolecules. DMSO alone had no effect. The modulation of the EBF (imiquimod alone or with DMSO) was not associated with changes in gene expression or the epithelial distribution of the main tight junction-related proteins (occludin, tricellulin, claudin-2, claudin-3, junctional adhesion molecule 1 and Zonula occludens-1). No changes in the proglucagon expression were observed. These results show that TLR7 stimulation leads to the modulation of the colonic EBF, having beneficial or detrimental effects depending upon the state of the epithelium. The underlying mechanisms remain elusive, but seem independent of the modulation of the main tight junction-related proteins or the barrier-enhancer factor GLP-2. Full article
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