Role of passive and adaptive immunity in influencing enterocyte-specific gene expression.
Numerous genes expressed by intestinal epithelial cells are developmentally regulated, and the influence that adaptive (AI) and passive (PI) immunity have in controlling their expression has not been evaluated. In this study, we tested the hypothesis that both PI and AI influenced enterocyte gene expression by developing a breeding scheme that used T and B cell-deficient recombination-activating gene (RAG) mice. RNA was isolated from the liver and proximal/distal small intestine at various ages, and the steady-state levels of six different transcripts were evaluated by RNase protection assay. In wild-type (WT) pups, all transcripts [Fc receptor of the neonate (FcRn), polymeric IgA receptor (pIgR), GLUT5, lactase-phlorizin hydrolase (lactase), apical sodium-dependent bile acid transporter (ASBT), and Na+/glucose cotransporter (SGLT1)] studied were developmentally regulated at the time of weaning, and all transcripts except ASBT had the highest levels of expression in the proximal small intestine. In WT suckling pups reared in the absence of PI, pIgR mRNA levels were increased 100% during the early phase of development. In mice lacking AI, the expression of pIgR and lactase were significantly attenuated, whereas FcRn and GLUT5 levels were higher compared with WT mice. Finally, in the absence of both passive and active immunity, expression levels of pIgR and lactase were significantly lower than similarly aged WT mice. In summary, we report that the adaptive and passive immune status of mice influences steady-state mRNA levels of several important, developmentally regulated enterocyte genes during the suckling and weaning periods of life.
Jenkins
Shannon L
SL
Division of Neonatology, Department of Pediatrics, David Geffen School of Medicine, University of California, Los Angeles 90095, USA.
Wang
Jiafang
J
Vazir
Mukta
M
Vela
Jose
J
Sahagun
Omar
O
Gabbay
Peter
P
Hoang
Lisa
L
Diaz
Rosa L
RL
Aranda
Richard
R
Martín
Martín G
MG
D000818:Animals; D000833:Animals, Suckling; D001402:B-Lymphocytes / Q000276:immunology; D002352:Carrier Proteins / Q000235:genetics; D020895:Enterocytes / Q000737:chemistry / Q000276:immunology* / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental / Q000276:immunology*; D016654:Genes, RAG-1 / Q000235:genetics / Q000276:immunology; D051296:Glucose Transporter Type 5; D007109:Immunity; D007110:Immunity, Active / Q000502:physiology; D007112:Immunity, Maternally-Acquired / Q000502:physiology; D007421:Intestine, Small / Q000737:chemistry; D010694:Lactase-Phlorizin Hydrolase / Q000235:genetics; D008562:Membrane Glycoproteins / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009004:Monosaccharide Transport Proteins / Q000235:genetics; D029363:Organic Anion Transporters, Sodium-Dependent; D012333:RNA, Messenger / Q000032:analysis; D011961:Receptors, Fc / Q000235:genetics; D051269:Sodium-Glucose Transporter 1; D027981:Symporters; D013601:T-Lymphocytes / Q000276:immunology; D014886:Weaning
D002352:Carrier Proteins; D051296:Glucose Transporter Type 5; C045281:IgA receptor; D008562:Membrane Glycoproteins; D009004:Monosaccharide Transport Proteins; D029363:Organic Anion Transporters, Sodium-Dependent; D012333:RNA, Messenger; D011961:Receptors, Fc; C495675:Slc5a1 protein, mouse; D051269:Sodium-Glucose Transporter 1; D027981:Symporters; C071908:sodium-bile acid cotransporter; D010694:Lactase-Phlorizin Hydrolase