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Article: The prenatal porcine intestine has low transforming growth factor-beta ligand and receptor density and shows reduced trophic response to enteral diets

TitleThe prenatal porcine intestine has low transforming growth factor-beta ligand and receptor density and shows reduced trophic response to enteral diets
Authors
KeywordsAmniotic fluid
Colostrum
Fetus
Milk
Mucosal immunity
Newborn
Issue Date2009
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpregu.physiology.org
Citation
American Journal Of Physiology - Regulatory Integrative And Comparative Physiology, 2009, v. 296 n. 4, p. R1053-R1062 How to Cite?
AbstractTransforming growth factor-beta (TGF-β) plays a role in enterocyte proliferation control, cell differentiation, and immune regulation via binding to specific TGF-β receptors (TGF-β R) in the intestinal epithelium. Endogenous TGF-β production is low in the intestine during the perinatal period, but some exogenous TGF-β ligands are supplied by amniotic fluid intake in the fetus and by colostrum ingestion in the neonate. It is not clear, however, whether luminal TGF-β receptors are present and functional at this critical time. We studied intestinal TGF-β receptors by immunohistochemistry during the last 20% of gestation in pigs and in chronically catheterized fetuses following exposure to colostrum, milk, and amniotic fluid (control). In fetal pigs, the TGF-β Rs were predominantly localized to the crypt epithelium, but staining intensity increased markedly just before term and shifted to the villous epithelium in newborn pigs, concurrently with marked increases in villous heights and crypt depths (+100-200%, P < 0.05). In contrast to previous observations in term newborn pigs, fetal pigs did not show any milk-induced change in TGF-β receptor densities or localization, although a moderate increase in villous height was observed, relative to control (+25-50%, P < 0.05). We conclude that intestinal TGF-β receptor density and localization are immature and unresponsive to TGF-β containing milk diets in prenatal pigs. Immaturity of TGF-β-mediated immune regulation may play a role in the increased sensitivity of preterm neonates to diet-induced intestinal inflammatory disorders. Copyright © 2009 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/60693
ISSN
2015 Impact Factor: 3.168
2015 SCImago Journal Rankings: 1.663
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSangild, PTen_HK
dc.contributor.authorMei, Jen_HK
dc.contributor.authorFowden, ALen_HK
dc.contributor.authorXu, RJen_HK
dc.date.accessioned2010-05-31T04:16:37Z-
dc.date.available2010-05-31T04:16:37Z-
dc.date.issued2009en_HK
dc.identifier.citationAmerican Journal Of Physiology - Regulatory Integrative And Comparative Physiology, 2009, v. 296 n. 4, p. R1053-R1062en_HK
dc.identifier.issn0363-6119en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60693-
dc.description.abstractTransforming growth factor-beta (TGF-β) plays a role in enterocyte proliferation control, cell differentiation, and immune regulation via binding to specific TGF-β receptors (TGF-β R) in the intestinal epithelium. Endogenous TGF-β production is low in the intestine during the perinatal period, but some exogenous TGF-β ligands are supplied by amniotic fluid intake in the fetus and by colostrum ingestion in the neonate. It is not clear, however, whether luminal TGF-β receptors are present and functional at this critical time. We studied intestinal TGF-β receptors by immunohistochemistry during the last 20% of gestation in pigs and in chronically catheterized fetuses following exposure to colostrum, milk, and amniotic fluid (control). In fetal pigs, the TGF-β Rs were predominantly localized to the crypt epithelium, but staining intensity increased markedly just before term and shifted to the villous epithelium in newborn pigs, concurrently with marked increases in villous heights and crypt depths (+100-200%, P < 0.05). In contrast to previous observations in term newborn pigs, fetal pigs did not show any milk-induced change in TGF-β receptor densities or localization, although a moderate increase in villous height was observed, relative to control (+25-50%, P < 0.05). We conclude that intestinal TGF-β receptor density and localization are immature and unresponsive to TGF-β containing milk diets in prenatal pigs. Immaturity of TGF-β-mediated immune regulation may play a role in the increased sensitivity of preterm neonates to diet-induced intestinal inflammatory disorders. Copyright © 2009 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpregu.physiology.orgen_HK
dc.relation.ispartofAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiologyen_HK
dc.subjectAmniotic fluiden_HK
dc.subjectColostrumen_HK
dc.subjectFetusen_HK
dc.subjectMilken_HK
dc.subjectMucosal immunityen_HK
dc.subjectNewbornen_HK
dc.titleThe prenatal porcine intestine has low transforming growth factor-beta ligand and receptor density and shows reduced trophic response to enteral dietsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6119&volume=296&spage=1053&epage=1062&date=2009&atitle=The+prenatal+porcine+intestine+has+low+transforming+growth+factor-beta+ligand+and+receptor+density+and+shows+reduced+trophic+response+to+enteral+dietsen_HK
dc.identifier.emailXu, RJ: xuruojun@hkucc.hku.hken_HK
dc.identifier.authorityXu, RJ=rp00820en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1152/ajpregu.90790.2008en_HK
dc.identifier.pmid19158412-
dc.identifier.scopuseid_2-s2.0-65949093030en_HK
dc.identifier.hkuros163546en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65949093030&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume296en_HK
dc.identifier.issue4en_HK
dc.identifier.spageR1053en_HK
dc.identifier.epageR1062en_HK
dc.identifier.isiWOS:000264565100024-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridSangild, PT=7004115316en_HK
dc.identifier.scopusauthoridMei, J=36857285200en_HK
dc.identifier.scopusauthoridFowden, AL=7006204534en_HK
dc.identifier.scopusauthoridXu, RJ=7402813973en_HK

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