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Journal ArticleDOI

Mechanisms of intestinal tight junctional disruption during infection.

O'Hara, +1 more
- 01 May 2008 - 
- Vol. 13, pp 7008-7021
TLDR
The mechanisms whereby select enteric viruses, bacterial pathogens and parasites modulate intestinal tight junctional structure and function are given and how these effects may contribute to the development of chronic intestinal disorders are given.
Abstract
Tight junctions are dynamic structures that may undergo structural and functional changes in response to both physiological and pathological circumstances. Several microbial pathogens impair intestinal barrier function by exploiting tight junctions. These pathogens have developed a broad and complex range of strategies to subvert host tight junction barrier function. The purpose of this review is to give an overview of the mechanisms whereby select enteric viruses, bacterial pathogens and parasites modulate intestinal tight junctional structure and function and how these effects may contribute to the development of chronic intestinal disorders.

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Citations
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Journal ArticleDOI

The small GTP-binding protein rho regulates the assembly of focal adhesions and actin stress fibers in response to growth factors

TL;DR: In this paper, rho, a ras-related GTP-binding protein, rapidly stimulated stress fiber and focal adhesion formation when microinjected into serum-starved Swiss 3T3 cells.
Journal ArticleDOI

Homeostasis and Inflammation in the Intestine

TL;DR: This Review considers the many cellular and molecular methods by which inflammatory responses are regulated to maintain intestinal homeostasis and the disease states that can ensue when this balance is lost.
Journal ArticleDOI

Extra-intestinal and long term consequences of Giardia duodenalis infections

TL;DR: A state-of-the-art discussion on the long-term consequences of Giardia infections, from extra-intestinal manifestations, growth and cognitive deficiencies, to post-infectious irritable bowel syndrome is offered.
Journal ArticleDOI

Cytoskeletal Regulation of Epithelial Barrier Function During Inflammation

TL;DR: This review highlights molecular events that lead to disruption of epithelial junctions during inflammation and focuses on key mechanisms of junctional regulation that are dependent on reorganization of the perijunctional F-actin cytoskeleton.
References
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Journal ArticleDOI

Rho GTPases and the Actin Cytoskeleton

TL;DR: Members of the Rho family of small guanosine triphosphatases have emerged as key regulators of the actin cytoskeleton, and through their interaction with multiple target proteins, they ensure coordinated control of other cellular activities such as gene transcription and adhesion.
Journal ArticleDOI

The small GTP-binding protein rho regulates the assembly of focal adhesions and actin stress fibers in response to growth factors.

Anne J. Ridley, +1 more
- 07 Aug 1992 - 
TL;DR: Rho, a ras-related GTP-binding protein, rapidly stimulated stress fiber and focal adhesion formation when microinjected into serum-starved Swiss 3T3 cells, implying that rho is essential specifically for the coordinated assembly of focal adhesions and stress fibers induced by growth factors.
Journal ArticleDOI

Isolation of a Common Receptor for Coxsackie B Viruses and Adenoviruses 2 and 5

TL;DR: Identification of CAR as a receptor for these two unrelated and structurally distinct viral pathogens is important for understanding viral pathogenesis and has implications for therapeutic gene delivery with adenovirus vectors.
Journal ArticleDOI

The tight junction: a multifunctional complex.

TL;DR: A group of integral membrane proteins-occludin, claudins, and junction adhesion molecules-interact with an increasingly complex array of tight junction plaque proteins not only to regulate paracellular solute and water flux but also to integrate such diverse processes as gene transcription, tumor suppression, cell proliferation, and cell polarity.
Journal ArticleDOI

Type III Secretion Machines: Bacterial Devices for Protein Delivery into Host Cells

TL;DR: Several Gram-negative pathogenic bacteria have evolved a complex protein secretion system termed type III to deliver bacterial effector proteins into host cells that then modulate host cellular functions.
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