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Innate immune cell–epithelial crosstalk during wound repair
Jennifer C. Brazil, … , Asma Nusrat, Charles A. Parkos
Jennifer C. Brazil, … , Asma Nusrat, Charles A. Parkos
Published July 22, 2019
Citation Information: J Clin Invest. 2019;129(8):2983-2993. https://doi.org/10.1172/JCI124618.
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Review Series

Innate immune cell–epithelial crosstalk during wound repair

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Abstract

Skin and intestinal epithelial barriers play a pivotal role in protecting underlying tissues from harsh external environments. The protective role of these epithelia is, in part, dependent on a remarkable capacity to restore barrier function and tissue homeostasis after injury. In response to damage, epithelial wounds repair by a series of events that integrate epithelial responses with those of resident and infiltrating immune cells including neutrophils and monocytes/macrophages. Compromise of this complex interplay predisposes to development of chronic nonhealing wounds, contributing to morbidity and mortality of many diseases. Improved understanding of crosstalk between epithelial and immune cells during wound repair is necessary for development of better pro-resolving strategies to treat debilitating complications of disorders ranging from inflammatory bowel disease to diabetes. In this Review we focus on epithelial and innate immune cell interactions that mediate wound healing and restoration of tissue homeostasis in the skin and intestine.

Authors

Jennifer C. Brazil, Miguel Quiros, Asma Nusrat, Charles A. Parkos

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Figure 1

Epithelial reparative triggers and events.

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Epithelial reparative triggers and events.
Cytokines, growth factors, Wn...
Cytokines, growth factors, Wnt ligands, SPMs, and MMPs released in the wound microenvironment in response to injury support epithelial cell proliferation as well as migration. Dynamic remodeling of focal adhesion complexes and actin promotes interactions with the ECM that facilitate the epithelial sheet’s migration. Following initial epithelial cell migration, keratinocytes peripheral to the leading edge proliferate and mature to restore epithelial barrier homeostasis and function.
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