Epithelial crosstalk at the microbiota-mucosal interface
This article provides an overview of how intestinal epithelial cells (IEC) recognize commensals and how they maintain host-bacterial symbiosis. Endocrine, goblet cells, and enterocytes of the intestinal epithelium express a range of pattern recognition receptors (PRR) to sense the presence of microbes. The best characterized are the Toll-like receptors (TLR) and nucleotide oligomerization domain-like receptors (NLR), which play a key role in pathogen recognition and the induction of innate effectors and inflammation. Several adaptations of PRR signaling have evolved in the gut to avoid uncontrolled and potentially destructive inflammatory responses toward the resident microbiota. PRR signaling in IEC serve to maintain the barrier functions of the epithelium, including the production of secretory IgA (sIgA). Additionally, IECs play a cardinal role in setting the immunosuppressive tone of the mucosa to inhibit overreaction against innocuous luminal antigens. This includes regulation of dendritic cells (DC), macrophage and lymphocyte functions by epithelial secreted cytokines. These immune mechanisms depend heavily on IEC recognition of microbes and are consistent with several studies in knockout mice that demonstrate TLR signaling in the epithelium has a profoundly beneficial role in maintaining homeostasis
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Format: | Article/Letter to editor biblioteca |
Language: | English |
Subjects: | antigen-presenting cells, crohns-disease, factor-kappa-b, growth-factor-beta, immune-response, intestinal dendritic cells, lamina propria, paneth cells, stromal cells, toll-like receptor-4, |
Online Access: | https://research.wur.nl/en/publications/epithelial-crosstalk-at-the-microbiota-mucosal-interface |
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dig-wur-nl-wurpubs-4269012024-09-30 Wells, J. Rossi, O. Meijerink, M. van Baarlen, P. Article/Letter to editor Proceedings of the National Academy of Sciences of the United States of America 108 (2011) Suppl. 1 ISSN: 0027-8424 Epithelial crosstalk at the microbiota-mucosal interface 2011 This article provides an overview of how intestinal epithelial cells (IEC) recognize commensals and how they maintain host-bacterial symbiosis. Endocrine, goblet cells, and enterocytes of the intestinal epithelium express a range of pattern recognition receptors (PRR) to sense the presence of microbes. The best characterized are the Toll-like receptors (TLR) and nucleotide oligomerization domain-like receptors (NLR), which play a key role in pathogen recognition and the induction of innate effectors and inflammation. Several adaptations of PRR signaling have evolved in the gut to avoid uncontrolled and potentially destructive inflammatory responses toward the resident microbiota. PRR signaling in IEC serve to maintain the barrier functions of the epithelium, including the production of secretory IgA (sIgA). Additionally, IECs play a cardinal role in setting the immunosuppressive tone of the mucosa to inhibit overreaction against innocuous luminal antigens. This includes regulation of dendritic cells (DC), macrophage and lymphocyte functions by epithelial secreted cytokines. These immune mechanisms depend heavily on IEC recognition of microbes and are consistent with several studies in knockout mice that demonstrate TLR signaling in the epithelium has a profoundly beneficial role in maintaining homeostasis en application/pdf https://research.wur.nl/en/publications/epithelial-crosstalk-at-the-microbiota-mucosal-interface 10.1073/pnas.1000092107 https://edepot.wur.nl/218961 antigen-presenting cells crohns-disease factor-kappa-b growth-factor-beta immune-response intestinal dendritic cells lamina propria paneth cells stromal cells toll-like receptor-4 (c) publisher Wageningen University & Research |
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antigen-presenting cells crohns-disease factor-kappa-b growth-factor-beta immune-response intestinal dendritic cells lamina propria paneth cells stromal cells toll-like receptor-4 antigen-presenting cells crohns-disease factor-kappa-b growth-factor-beta immune-response intestinal dendritic cells lamina propria paneth cells stromal cells toll-like receptor-4 |
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antigen-presenting cells crohns-disease factor-kappa-b growth-factor-beta immune-response intestinal dendritic cells lamina propria paneth cells stromal cells toll-like receptor-4 antigen-presenting cells crohns-disease factor-kappa-b growth-factor-beta immune-response intestinal dendritic cells lamina propria paneth cells stromal cells toll-like receptor-4 Wells, J. Rossi, O. Meijerink, M. van Baarlen, P. Epithelial crosstalk at the microbiota-mucosal interface |
description |
This article provides an overview of how intestinal epithelial cells (IEC) recognize commensals and how they maintain host-bacterial symbiosis. Endocrine, goblet cells, and enterocytes of the intestinal epithelium express a range of pattern recognition receptors (PRR) to sense the presence of microbes. The best characterized are the Toll-like receptors (TLR) and nucleotide oligomerization domain-like receptors (NLR), which play a key role in pathogen recognition and the induction of innate effectors and inflammation. Several adaptations of PRR signaling have evolved in the gut to avoid uncontrolled and potentially destructive inflammatory responses toward the resident microbiota. PRR signaling in IEC serve to maintain the barrier functions of the epithelium, including the production of secretory IgA (sIgA). Additionally, IECs play a cardinal role in setting the immunosuppressive tone of the mucosa to inhibit overreaction against innocuous luminal antigens. This includes regulation of dendritic cells (DC), macrophage and lymphocyte functions by epithelial secreted cytokines. These immune mechanisms depend heavily on IEC recognition of microbes and are consistent with several studies in knockout mice that demonstrate TLR signaling in the epithelium has a profoundly beneficial role in maintaining homeostasis |
format |
Article/Letter to editor |
topic_facet |
antigen-presenting cells crohns-disease factor-kappa-b growth-factor-beta immune-response intestinal dendritic cells lamina propria paneth cells stromal cells toll-like receptor-4 |
author |
Wells, J. Rossi, O. Meijerink, M. van Baarlen, P. |
author_facet |
Wells, J. Rossi, O. Meijerink, M. van Baarlen, P. |
author_sort |
Wells, J. |
title |
Epithelial crosstalk at the microbiota-mucosal interface |
title_short |
Epithelial crosstalk at the microbiota-mucosal interface |
title_full |
Epithelial crosstalk at the microbiota-mucosal interface |
title_fullStr |
Epithelial crosstalk at the microbiota-mucosal interface |
title_full_unstemmed |
Epithelial crosstalk at the microbiota-mucosal interface |
title_sort |
epithelial crosstalk at the microbiota-mucosal interface |
url |
https://research.wur.nl/en/publications/epithelial-crosstalk-at-the-microbiota-mucosal-interface |
work_keys_str_mv |
AT wellsj epithelialcrosstalkatthemicrobiotamucosalinterface AT rossio epithelialcrosstalkatthemicrobiotamucosalinterface AT meijerinkm epithelialcrosstalkatthemicrobiotamucosalinterface AT vanbaarlenp epithelialcrosstalkatthemicrobiotamucosalinterface |
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1813443202246508544 |