Format

Send to

Choose Destination
Gastroenterology. 2016 Dec;151(6):1087-1095. doi: 10.1053/j.gastro.2016.09.048. Epub 2016 Oct 8.

Innate Immune Cell Trafficking and Function During Sterile Inflammation of the Liver.

Author information

1
Department of Critical Care Medicine, University of Calgary, Calgary, Alberta, Canada; Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.
2
Department of Critical Care Medicine, University of Calgary, Calgary, Alberta, Canada; Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada; Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada. Electronic address: pkubes@ucalgary.ca.

Abstract

The sterile inflammatory response (inflammation in the absence of infection) to tissue injury and cell death is required for normal wound healing. However, dysregulated sterile inflammation leads to various acute and chronic inflammatory diseases, including those of the liver and gastrointestinal tract. It is therefore important to increase our understanding of the mechanisms that control physiological versus pathological sterile inflammation. We have begun to clarify the cellular and molecular mechanisms that coordinate the innate immune response to tissue damage and cell death in the liver. In this review, we summarize the mechanisms that alert the immune system to the presence of tissue damage and highlight recent advances in our understanding of innate immune cell trafficking to sites of hepatic sterile inflammation. We explore the functions of various innate immune cells in the coordination of tissue repair, including previously underappreciated roles of peritoneal macrophages and platelets. We propose that dysregulation of immune cell trafficking or function at sites of tissue injury contributes to the misdirection of sterile inflammation to promote chronic inflammatory disease.

KEYWORDS:

Leukocyte Trafficking; Sterile Inflammation; Tissue Repair

PMID:
27725145
DOI:
10.1053/j.gastro.2016.09.048
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center