Send to

Choose Destination
See comment in PubMed Commons below
Tissue Barriers. 2013 Apr 1;1(2):e24957. doi: 10.4161/tisb.24957.

Netrin-1 guides inflammatory cell migration to control mucosal immune responses during intestinal inflammation.

Author information

Mucosal Inflammation Program; Department of Anesthesiology and Perioperative Medicine; University of Colorado Anschutz Medical Campus; Aurora, CO USA.
Department of Pediatrics; Children's Hospital Colorado; Aurora, CO USA.


The intestinal epithelium is a dynamic barrier playing an active role in intestinal homeostasis and inflammation. Intestinal barrier function is dysregulated during inflammatory bowel disease (IBD), with epithelial cells playing a significant part in generating an inflammatory milieu through the release of signals that attract leukocytes to the intestinal lamina propria. However, it is increasingly appreciated that the intestinal epithelium mediates a counterbalancing response to drive resolution. Drawing analogies with neuronal development, where the balance of chemoattractive and chemorepellent signals is key to directed neuronal movement it has been postulated that such secreted cues play a role in leukocyte migration. Netrin-1 is one of the best-described neuronal guidance molecules, which has been shown to play a significant role in directed migration of leukocytes. Prior to our study the potential role of netrin-1 in IBD was poorly characterized. We defined netrin-1 as an intestinal epithelial-derived protein capable of limiting neutrophil recruitment to attenuate acute colitis. Our study highlights that the intestinal epithelium releases factors during acute inflammation that are responsible for fine-tuning the immune response. Exploration of these epithelial-mediated protective mechanisms will shed light on the complexity of the intestinal epithelial barrier in health and disease.


apoptosis; inflammatory bowel disease; intestinal epithelial cells; leukocyte migration; neuronal guidance molecule

PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis Icon for PubMed Central
    Loading ...
    Support Center