Mouse Genome Informatics
cx1
    Il6tm1Kopf/Il6tm1Kopf
Tg(ED-L2-IL1RN/IL1B)#Tcw/?

B6.Cg-Il6tm1Kopf Tg(ED-L2-IL1RN/IL1B)#Tcw
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
N
• absence of Il6 expression completely abolishes the metaplastic and dysplastic phenotypes seen in transgenic mice expressing Il6 (J:180282)
• minor inflammatory response

immune system
• minor inflammatory response

Mouse Models of Human Disease
OMIM IDRef(s)
NOT Barrett Esophagus 614266 J:180282


Mouse Genome Informatics
cx2
    Il6tm1Kopf/Il6+
Tg(ED-L2-IL1RN/IL1B)#Tcw/?

B6.Cg-Il6tm1Kopf Tg(ED-L2-IL1RN/IL1B)#Tcw
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
N
• reduced of Il6 expression completely decreases metaplasia and abolishes dysplasia (J:180282)

immune system


Mouse Genome Informatics
tg3
    Tg(ED-L2-IL1RN/IL1B)#Tcw/?
B6.Cg-Tg(ED-L2-IL1RN/IL1B)#Tcw
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• at 6 months of age profound epithelial hyperplasia is seen in the squamocolumnar junction
• at 12-15 months of age, 90% of mice display severe columnar metaplasia with mucus producing cells in the squamocolumnar junction
• treatment with 0.2% deoxycholate accelerates the development of Barrett-like metaplasia in the squamocolumnar junction
• at 20-22 months of age about 20% of mice develop high-grade dysplasia or intramucosal esophageal adenocarcinoma
• at 20-22 months of age lesions are grossly visible within the distal end of the esophagus
• mutant esophagi show circumferential erythema and edema with inflammatory exudates compared to the normal esophagus and changes are made more severe by treatment with 0.2% deoxycholate
• expansion of gastric cardia progenitor cells in the esophagus over time
• markedly thickened
• markedly thickened with a mix of acute and chronic inflammatory infiltrate
• markedly thickened forestomach with a mix of acute and chronic inflammatory infiltrate
• increase in proliferation in the esophageal basal compartment
• mix of acute and chronic inflammatory infiltrate
• treatment with 0.2% deoxycholate induced more severe esophagitis with inflammatory infiltrates in mutant mice compared to wild-type controls

tumorigenesis
• mice treated with 0.2% deoxycholate and N-methyl-N-nitrosourea show increased esophageal tumor development compared to wild-type controls
• at 20-22 months of age about 20% of mice develop high-grade dysplasia or intramucosal esophageal adenocarcinoma
• during the stepwise progression to cancer there is a gradual increase in alpha SMA+ stromal myofibroblasts and increasing stroma global hypomethylation

immune system
• elevated IL6 in the tongue, esophagus, and forestomach but not in the stomach
• mix of acute and chronic inflammatory infiltrate in the forestomach
• at 6 months of age moderate inflammation is seen in the squamocolumnar junction
• mix of acute and chronic inflammatory infiltrate
• treatment with 0.2% deoxycholate induced more severe esophagitis with inflammatory infiltrates in mutant mice compared to wild-type controls

homeostasis/metabolism
• elevated IL6 in the tongue, esophagus, and forestomach but not in the stomach
• mice treated with 0.2% deoxycholate and N-methyl-N-nitrosourea show increased esophageal tumor development compared to wild-type controls

growth/size/body
• at 20-22 months, associated with gross esophageal lesions

hematopoietic system

Mouse Models of Human Disease
OMIM IDRef(s)
Barrett Esophagus 614266 J:180282
Esophageal Cancer 133239 J:180282