Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota.Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium

Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota.Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium

Apoptosis, necrosis, and necroptosis in the gut and intestinal homeostasis / Negroni, Anna; Cucchiara, Salvatore; Stronati, Laura. - In: MEDIATORS OF INFLAMMATION. - ISSN 0962-9351. - ELETTRONICO. - 2015:(2015). [10.1155/2015/250762]

Apoptosis, necrosis, and necroptosis in the gut and intestinal homeostasis

CUCCHIARA, Salvatore;STRONATI, LAURA
2015

Abstract

Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota.Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium
2015
Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota.Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium
Immunology; Cell Biology
01 Pubblicazione su rivista::01a Articolo in rivista
Apoptosis, necrosis, and necroptosis in the gut and intestinal homeostasis / Negroni, Anna; Cucchiara, Salvatore; Stronati, Laura. - In: MEDIATORS OF INFLAMMATION. - ISSN 0962-9351. - ELETTRONICO. - 2015:(2015). [10.1155/2015/250762]
File allegati a questo prodotto
File Dimensione Formato  
Negroni_Apoptosis_2015.pdf

accesso aperto

Tipologia: Documento in Post-print (versione successiva alla peer review e accettata per la pubblicazione)
Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 706.08 kB
Formato Adobe PDF
706.08 kB Adobe PDF

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/837831
Citazioni
  • ???jsp.display-item.citation.pmc??? 62
  • Scopus 122
  • ???jsp.display-item.citation.isi??? 112
social impact