Ganong's Review of Medical Physiology
- K. Barrett
- Medicine, Biology
- 2010
This chapter discusses the regulation of endocrine functions of the pituitary gland, which governs the development & function of the female reproductive system and the male reproductive system.
Chloride secretion by the intestinal epithelium: molecular basis and regulatory aspects.
- K. Barrett, S. Keely
- BiologyAnnual Review of Physiology
- 2000
This article reviews the area of investigation in chloride transport, with an emphasis on recent developments and their implications for the physiology and pathophysiology of chloride transport.
Live probiotics protect intestinal epithelial cells from the effects of infection with enteroinvasive Escherichia coli (EIEC)
- S. Resta-Lenert, K. Barrett
- Biology, MedicineGut
- 1 July 2003
Live ST/LA interact with intestinal epithelial cells to protect them from the deleterious effect of EIEC via mechanisms that include, but are not limited to, interference with pathogen adhesion and invasion.
Probiotics and commensals reverse TNF-alpha- and IFN-gamma-induced dysfunction in human intestinal epithelial cells.
- S. Resta-Lenert, K. Barrett
- Biology, MedicineGastroenterology
- 2006
Litterious effects of TNF-alpha and IFN-gamma on epithelial function are prevented by probiotic, and to a lesser extent, commensal pretreatment, and may justify their use in inflammatory disorders.
Gs Protein-coupled Receptor Agonists Induce Transactivation of the Epidermal Growth Factor Receptor in T84 Cells
- L. Bertelsen, K. Barrett, S. Keely
- BiologyJournal of Biological Chemistry
- 20 February 2004
GsPCR agonists rapidly transactivate the EGFr in T84 cells by a signaling pathway involving cAMP and PKA, through a mechanism that likely involves PI3K, which is required for the full expression of cAMP-dependent Cl- secretory responses.
Transactivation of the Epidermal Growth Factor Receptor in Colonic Epithelial Cells by Carbachol Requires Extracellular Release of Transforming Growth Factor-α*
- D. Mccole, S. Keely, R. Coffey, K. Barrett
- BiologyJournal of Biological Chemistry
- 8 November 2002
CCh-stimulated EGFr transactivation and subsequent ERK activation, a pathway that limits CCh-induced chloride secretion, is mediated by metalloproteinase-dependent extracellular release of TGF-α and intracellular Src activation.
Probiotics and Commensals Reverse TNF-α– and IFN-γ–Induced Dysfunction in Human Intestinal Epithelial Cells
- S. Resta-Lenert, K. Barrett
- Biology, Medicine
- 1 April 2003
Background & Aims: Commensal bacteria are crucial for the development of the mucosal immune system. Probiotics are commensals with special characteristics and may protect mucosal surfaces against…
Positive and negative regulation of chloride secretion in T84 cells.
- K. Barrett
- BiologyAmerican Journal of Physiology
- 1 October 1993
This review discusses recent findings regarding the mechanisms and regulation of chloride secretion in the T84 cell line, a widely used model for the study of transepithelial chloride transport, the properties of the cystic fibrosis gene product, and the interactions of inflammatory cell types with the intestinal epithelium.
Role of intestinal epithelial cells in the host secretory response to infection by invasive bacteria. Bacterial entry induces epithelial prostaglandin h synthase-2 expression and prostaglandin E2 and…
- L. Eckmann, W. Stenson, M. Kagnoff
- Biology, MedicineJournal of Clinical Investigation
- 15 July 1997
A novel autocrine/paracrine function of mediators produced by intestinal epithelial cells in the rapid induction of increased fluid secretion in response to intestinal infection with invasive bacteria is defined.
Carbachol stimulates transactivation of epidermal growth factor receptor and mitogen-activated protein kinase in T84 cells. Implications for carbachol-stimulated chloride secretion.
- S. Keely, J. Uribe, K. Barrett
- BiologyJournal of Biological Chemistry
- 16 October 1998
It is concluded that CCh activates ERK in T84 cells via a mechanism involving transactivation of the EGFr, and that this pathway constitutes an inhibitory signaling pathway by which chloride secretory responses to CCh may be negatively regulated.
...
...