Next Article in Journal
Anti-Inflammatory Effect of Sulforaphane on LPS-Activated Microglia Potentially through JNK/AP-1/NF-κB Inhibition and Nrf2/HO-1 Activation
Next Article in Special Issue
Lack of Small Intestinal Dysbiosis Following Long-Term Selective Inhibition of Cyclooxygenase-2 by Rofecoxib in the Rat
Previous Article in Journal
In-Depth Proteome Analysis Highlights HepaRG Cells as a Versatile Cell System Surrogate for Primary Human Hepatocytes
Previous Article in Special Issue
Crohn’s Disease Patients in Remission Display an Enhanced Intestinal IgM+ B Cell Count in Concert with a Strong Activation of the Intestinal Complement System
Review

Cellular and Molecular Therapeutic Targets in Inflammatory Bowel Disease—Focusing on Intestinal Barrier Function

1
School of Medical Sciences, Örebro University, 703 62 Örebro, Sweden
2
Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics & Oncology, Medical Faculty, Linköping University, 581 85 Linköping, Sweden
*
Author to whom correspondence should be addressed.
Cells 2019, 8(2), 193; https://doi.org/10.3390/cells8020193
Received: 20 January 2019 / Revised: 18 February 2019 / Accepted: 21 February 2019 / Published: 22 February 2019
The human gut relies on several cellular and molecular mechanisms to allow for an intact and dynamical intestinal barrier. Normally, only small amounts of luminal content pass the mucosa, however, if the control is broken it can lead to enhanced passage, which might damage the mucosa, leading to pathological conditions, such as inflammatory bowel disease (IBD). It is well established that genetic, environmental, and immunological factors all contribute in the pathogenesis of IBD, and a disturbed intestinal barrier function has become a hallmark of the disease. Genetical studies support the involvement of intestinal barrier as several susceptibility genes for IBD encode proteins with key functions in gut barrier and homeostasis. IBD patients are associated with loss in bacterial diversity and shifts in the microbiota, with a possible link to local inflammation. Furthermore, alterations of immune cells and several neuro-immune signaling pathways in the lamina propria have been demonstrated. An inappropriate immune activation might lead to mucosal inflammation, with elevated secretion of pro-inflammatory cytokines that can affect the epithelium and promote a leakier barrier. This review will focus on the main cells and molecular mechanisms in IBD and how these can be targeted in order to improve intestinal barrier function and reduce inflammation. View Full-Text
Keywords: Crohn’s disease; ulcerative colitis; intestinal permeability therapeutic targets; innate and adaptive immunity Crohn’s disease; ulcerative colitis; intestinal permeability therapeutic targets; innate and adaptive immunity
Show Figures

Graphical abstract

MDPI and ACS Style

Schoultz, I.; Keita, Å.V. Cellular and Molecular Therapeutic Targets in Inflammatory Bowel Disease—Focusing on Intestinal Barrier Function. Cells 2019, 8, 193. https://doi.org/10.3390/cells8020193

AMA Style

Schoultz I, Keita ÅV. Cellular and Molecular Therapeutic Targets in Inflammatory Bowel Disease—Focusing on Intestinal Barrier Function. Cells. 2019; 8(2):193. https://doi.org/10.3390/cells8020193

Chicago/Turabian Style

Schoultz, Ida, and Åsa V. Keita. 2019. "Cellular and Molecular Therapeutic Targets in Inflammatory Bowel Disease—Focusing on Intestinal Barrier Function" Cells 8, no. 2: 193. https://doi.org/10.3390/cells8020193

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop