TGFβ1 single-nucleotide polymorphism C-509T alters mucosal cell function in pediatric eosinophilic esophagitis

Eosinophilic esophagitis (EoE) is a chronic Th2 antigen-driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal rigidity, strictures, and dysphagia. TGFβ1 drives esophageal remodeling including epithelial barrier dysfunction and subepithelial fibrosis. A fun...

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Vydané v:Mucosal immunology Ročník 13; číslo 1; s. 110 - 117
Hlavní autori: Duong, L.D., Rawson, R., Bezryadina, A., Manresa, M.C., Newbury, R.O., Dohil, R., Liu, Z., Barrett, K., Kurten, R., Aceves, S.S.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: New York Elsevier Inc 01.01.2020
Nature Publishing Group US
Elsevier Limited
Predmet:
Allergology
Antibodies
Autoimmune diseases
Biomedical and Life Sciences
Biomedicine
Biopsy
Cell Adhesion
Cells, Cultured
Child
Collagen
Contractility
Dysphagia
E-cadherin
Eosinophilic Esophagitis - genetics
Eosinophilic Esophagitis - immunology
Epithelial cells
Epithelial Cells - physiology
Esophageal diseases
Esophagitis
Esophagus
Female
Fibroblasts
Fibroblasts - physiology
Fibrosis
Gastroenterology
Gastrointestinal diseases
Gelatinase A
Gene expression
Gene polymorphism
Genetic Association Studies
Genotype
Genotype & phenotype
Humans
Immunology
Inflammation
Intestinal Mucosa - immunology
Intestinal Mucosa - pathology
Leukocytes (eosinophilic)
Localization
Lymphocytes T
Male
Mucosa
Polymorphism, Single Nucleotide
Single-nucleotide polymorphism
Spheroids
Stricture
Transcription
Transforming Growth Factor beta1 - genetics
Transforming growth factor-b1
ISSN:1933-0219, 1935-3456, 1935-3456
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Abstract Eosinophilic esophagitis (EoE) is a chronic Th2 antigen-driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal rigidity, strictures, and dysphagia. TGFβ1 drives esophageal remodeling including epithelial barrier dysfunction and subepithelial fibrosis. A functional SNP in the TGFβ1 gene that increases its transcription (C-509T) is associated with elevated numbers of esophageal TGFβ1-expressing cells. We utilized esophageal biopsies and fibroblasts from TT-genotype EoE children to understand if TGFβ1 influenced fibroblast and epithelial cell function in vivo. Genotype TT EoE esophageal fibroblasts had higher baseline TGFβ1, collagen1α1, periostin, and MMP2 (p < 0.05) gene expression and distinct contractile properties compared with CC genotype (n = 6 subjects per genotype). In vitro TGFβ1 exposure caused greater induction of target gene expression in genotype CC fibroblasts (p < 0.05). Esophageal biopsies from TT-genotype subjects had significantly less epithelial membrane-bound E-cadherin (p < 0.01) and wider cluster distribution at nanometer resolution. TGFβ1 treatment of stratified primary human esophageal epithelial cells and spheroids disrupted transepithelial resistance (p < 0.001) and E-cadherin localization (p < 0.0001). A TGFβ1-receptor-I inhibitor improved TGFβ1-mediated E-cadherin mislocalization. These data suggest that EoE severity can depend on genotypic differences that increase in vivo exposure to TGFβ1. TGFβ1 inhibition may be a useful therapy in subsets of EoE patients.
AbstractList Eosinophilic esophagitis (EoE) is a chronic Th2 antigen driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal rigidity, strictures, and dysphagia. TGFβ1 drives esophageal remodeling including epithelial barrier dysfunction and subepithelial fibrosis. A functional SNP in the TGFβ1 gene that increases its transcription (C-509T) associates with elevated numbers of esophageal TGFβ1 expressing cells. We utilized esophageal biopsies and fibroblasts from TT genotype EoE children to understand if TGFβ1 influenced fibroblast and epithelial cell function in vivo. Genotype TT EoE esophageal fibroblasts had higher baseline TGFβ1, collagen1α1, periostin, and MMP-2 (p<.05) gene expression and distinct contractile properties compared with CC genotype (n=6 subjects per genotype). In vitro TGFβ1 exposure caused greater induction of target gene expression in genotype CC fibroblasts (p<.05). Esophageal biopsies from TT genotype subjects had significantly less epithelial membrane bound E-cadherin (p<.01) and wider cluster distribution at nanometer resolution. TGFβ1 treatment of stratified primary human esophageal epithelial cells and spheroids disrupted transepithelial resistance (p<.001) and E-cadherin localization (p<.0001). A TGFβ1-receptor-I inhibitor improved TGFβ1-mediated E-cadherin mislocalization. These data suggest that EoE severity can depend on genotypic differences that increase in vivo exposure to TGFβ1. TGFβ1 inhibition may be a useful therapy in subsets of EoE patients.
Eosinophilic esophagitis (EoE) is a chronic Th2 antigen-driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal rigidity, strictures, and dysphagia. TGFβ1 drives esophageal remodeling including epithelial barrier dysfunction and subepithelial fibrosis. A functional SNP in the TGFβ1 gene that increases its transcription (C-509T) is associated with elevated numbers of esophageal TGFβ1-expressing cells. We utilized esophageal biopsies and fibroblasts from TT-genotype EoE children to understand if TGFβ1 influenced fibroblast and epithelial cell function in vivo. Genotype TT EoE esophageal fibroblasts had higher baseline TGFβ1, collagen1α1, periostin, and MMP2 (p < 0.05) gene expression and distinct contractile properties compared with CC genotype (n = 6 subjects per genotype). In vitro TGFβ1 exposure caused greater induction of target gene expression in genotype CC fibroblasts (p < 0.05). Esophageal biopsies from TT-genotype subjects had significantly less epithelial membrane-bound E-cadherin (p < 0.01) and wider cluster distribution at nanometer resolution. TGFβ1 treatment of stratified primary human esophageal epithelial cells and spheroids disrupted transepithelial resistance (p < 0.001) and E-cadherin localization (p < 0.0001). A TGFβ1-receptor-I inhibitor improved TGFβ1-mediated E-cadherin mislocalization. These data suggest that EoE severity can depend on genotypic differences that increase in vivo exposure to TGFβ1. TGFβ1 inhibition may be a useful therapy in subsets of EoE patients.
Eosinophilic esophagitis (EoE) is a chronic Th2 antigen-driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal rigidity, strictures, and dysphagia. TGFβ1 drives esophageal remodeling including epithelial barrier dysfunction and subepithelial fibrosis. A functional SNP in the TGFβ1 gene that increases its transcription (C-509T) is associated with elevated numbers of esophageal TGFβ1-expressing cells. We utilized esophageal biopsies and fibroblasts from TT-genotype EoE children to understand if TGFβ1 influenced fibroblast and epithelial cell function in vivo. Genotype TT EoE esophageal fibroblasts had higher baseline TGFβ1, collagen1α1, periostin, and MMP2 (p < 0.05) gene expression and distinct contractile properties compared with CC genotype (n = 6 subjects per genotype). In vitro TGFβ1 exposure caused greater induction of target gene expression in genotype CC fibroblasts (p < 0.05). Esophageal biopsies from TT-genotype subjects had significantly less epithelial membrane-bound E-cadherin (p < 0.01) and wider cluster distribution at nanometer resolution. TGFβ1 treatment of stratified primary human esophageal epithelial cells and spheroids disrupted transepithelial resistance (p < 0.001) and E-cadherin localization (p < 0.0001). A TGFβ1-receptor-I inhibitor improved TGFβ1-mediated E-cadherin mislocalization. These data suggest that EoE severity can depend on genotypic differences that increase in vivo exposure to TGFβ1. TGFβ1 inhibition may be a useful therapy in subsets of EoE patients.Eosinophilic esophagitis (EoE) is a chronic Th2 antigen-driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal rigidity, strictures, and dysphagia. TGFβ1 drives esophageal remodeling including epithelial barrier dysfunction and subepithelial fibrosis. A functional SNP in the TGFβ1 gene that increases its transcription (C-509T) is associated with elevated numbers of esophageal TGFβ1-expressing cells. We utilized esophageal biopsies and fibroblasts from TT-genotype EoE children to understand if TGFβ1 influenced fibroblast and epithelial cell function in vivo. Genotype TT EoE esophageal fibroblasts had higher baseline TGFβ1, collagen1α1, periostin, and MMP2 (p < 0.05) gene expression and distinct contractile properties compared with CC genotype (n = 6 subjects per genotype). In vitro TGFβ1 exposure caused greater induction of target gene expression in genotype CC fibroblasts (p < 0.05). Esophageal biopsies from TT-genotype subjects had significantly less epithelial membrane-bound E-cadherin (p < 0.01) and wider cluster distribution at nanometer resolution. TGFβ1 treatment of stratified primary human esophageal epithelial cells and spheroids disrupted transepithelial resistance (p < 0.001) and E-cadherin localization (p < 0.0001). A TGFβ1-receptor-I inhibitor improved TGFβ1-mediated E-cadherin mislocalization. These data suggest that EoE severity can depend on genotypic differences that increase in vivo exposure to TGFβ1. TGFβ1 inhibition may be a useful therapy in subsets of EoE patients.
Eosinophilic esophagitis (EoE) is a chronic Th2 antigen-driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal rigidity, strictures, and dysphagia. TGFβ1 drives esophageal remodeling including epithelial barrier dysfunction and subepithelial fibrosis. A functional SNP in the TGFβ1 gene that increases its transcription (C-509T) is associated with elevated numbers of esophageal TGFβ1-expressing cells. We utilized esophageal biopsies and fibroblasts from TT-genotype EoE children to understand if TGFβ1 influenced fibroblast and epithelial cell function in vivo. Genotype TT EoE esophageal fibroblasts had higher baseline TGFβ1, collagen1α1, periostin, and MMP2 ( p  < 0.05) gene expression and distinct contractile properties compared with CC genotype ( n  = 6 subjects per genotype). In vitro TGFβ1 exposure caused greater induction of target gene expression in genotype CC fibroblasts ( p  < 0.05). Esophageal biopsies from TT-genotype subjects had significantly less epithelial membrane-bound E-cadherin ( p  < 0.01) and wider cluster distribution at nanometer resolution. TGFβ1 treatment of stratified primary human esophageal epithelial cells and spheroids disrupted transepithelial resistance ( p  < 0.001) and E-cadherin localization ( p  < 0.0001). A TGFβ1-receptor-I inhibitor improved TGFβ1-mediated E-cadherin mislocalization. These data suggest that EoE severity can depend on genotypic differences that increase in vivo exposure to TGFβ1. TGFβ1 inhibition may be a useful therapy in subsets of EoE patients.
Author Newbury, R.O.
Rawson, R.
Bezryadina, A.
Barrett, K.
Aceves, S.S.
Manresa, M.C.
Kurten, R.
Dohil, R.
Liu, Z.
Duong, L.D.
AuthorAffiliation 3 Department of Bioengineering, University of California, San Diego
7 Arkansas Children’s Research Institute and University of Arkansas for Medical Sciences, Little Rock, Arkansas
6 Department of Medicine, University of California, San Diego
4 Department of Pathology, University of California, San Diego, Rady Children’s Hospital, San Diego
5 Division of Gastroenterology
2 Department of Pediatrics, University of California, San Diego and Rady Children’s Hospital San Diego
1 Division of Allergy & Immunology, University of California, San Diego and Rady Children’s Hospital San Diego
AuthorAffiliation_xml – name: 6 Department of Medicine, University of California, San Diego
– name: 2 Department of Pediatrics, University of California, San Diego and Rady Children’s Hospital San Diego
– name: 1 Division of Allergy & Immunology, University of California, San Diego and Rady Children’s Hospital San Diego
– name: 3 Department of Bioengineering, University of California, San Diego
– name: 4 Department of Pathology, University of California, San Diego, Rady Children’s Hospital, San Diego
– name: 5 Division of Gastroenterology
– name: 7 Arkansas Children’s Research Institute and University of Arkansas for Medical Sciences, Little Rock, Arkansas
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RK: Provided samples, analyzed data, critically reviewed the manuscript
LDD: Designed, performed, and analyzed experiments and data, assisted in manuscript preparation, and critically reviewed the manuscript
RR: Designed, performed, and analyzed experiments and data, assisted in manuscript preparation, and critically reviewed the manuscript
SSA: Designed experiments, procured funding, analyzed experimental data, wrote the manuscript
AB: Designed, performed, and analyzed experiments and data, assisted in manuscript preparation, and critically reviewed the manuscript
Author Contributions
ZL: Provided essential expertise, analyzed data, critically reviewed the manuscript
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PublicationCentury 2000
PublicationDate 20200100
PublicationDateYYYYMMDD 2020-01-01
PublicationDate_xml – month: 1
  year: 2020
  text: 20200100
PublicationDecade 2020
PublicationPlace New York
PublicationPlace_xml – name: New York
– name: United States
– name: Kidlington
PublicationSubtitle The official publication of the Society for Mucosal Immunology
PublicationTitle Mucosal immunology
PublicationTitleAbbrev Mucosal Immunol
PublicationTitleAlternate Mucosal Immunol
PublicationYear 2020
Publisher Elsevier Inc
Nature Publishing Group US
Elsevier Limited
Publisher_xml – name: Elsevier Inc
– name: Nature Publishing Group US
– name: Elsevier Limited
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Snippet Eosinophilic esophagitis (EoE) is a chronic Th2 antigen-driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal...
Eosinophilic esophagitis (EoE) is a chronic Th2 antigen driven disorder associated with tissue remodeling. Inflammation and remodeling lead to esophageal...
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proquest
pubmed
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springer
elsevier
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 110
SubjectTerms Allergology
Antibodies
Autoimmune diseases
Biomedical and Life Sciences
Biomedicine
Biopsy
Cell Adhesion
Cells, Cultured
Child
Collagen
Contractility
Dysphagia
E-cadherin
Eosinophilic Esophagitis - genetics
Eosinophilic Esophagitis - immunology
Epithelial cells
Epithelial Cells - physiology
Esophageal diseases
Esophagitis
Esophagus
Female
Fibroblasts
Fibroblasts - physiology
Fibrosis
Gastroenterology
Gastrointestinal diseases
Gelatinase A
Gene expression
Gene polymorphism
Genetic Association Studies
Genotype
Genotype & phenotype
Humans
Immunology
Inflammation
Intestinal Mucosa - immunology
Intestinal Mucosa - pathology
Leukocytes (eosinophilic)
Localization
Lymphocytes T
Male
Mucosa
Polymorphism, Single Nucleotide
Single-nucleotide polymorphism
Spheroids
Stricture
Transcription
Transforming Growth Factor beta1 - genetics
Transforming growth factor-b1
Title TGFβ1 single-nucleotide polymorphism C-509T alters mucosal cell function in pediatric eosinophilic esophagitis
URI https://www.clinicalkey.com/#!/content/1-s2.0-S1933021922002458
https://link.springer.com/article/10.1038/s41385-019-0214-9
https://www.ncbi.nlm.nih.gov/pubmed/31636346
https://www.proquest.com/docview/2327331327
https://www.proquest.com/docview/2475031217
https://www.proquest.com/docview/2307727654
https://pubmed.ncbi.nlm.nih.gov/PMC6917872
Volume 13
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