Small GTPase-dependent regulation of leukocyte–endothelial interactions in inflammation

Julia Y. Chu, Barry Mccormick, Sonja Vermeren

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Abstract


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Inflammation is a complex biological response that serves to protect the body's tissues following harmful stimuli such as infection, irritation or injury and initiates tissue repair. At the start of an inflammatory response, pro-inflammatory mediators induce changes in the endothelial lining of the blood vessels and in leukocytes. This results in increased vascular permeability and increased expression of adhesion proteins, and promotes adhesion of leukocytes, especially neutrophils to the endothelium. Adhesion is a prerequisite for neutrophil extravasation and chemoattractant-stimulated recruitment to inflammatory sites, where neutrophils phagocytose and kill microbes, release inflammatory mediators and cross-talk with other immune cells to co-ordinate the immune response in preparation for tissue repair. Many signalling proteins are critically involved in the complex signalling processes that underpin the inflammatory response and cross-talk between endothelium and leukocytes. As key regulators of cell–cell and cell–substratum adhesion, small GTPases (guanosine triphosphatases) act as important controls of neutrophil-endothelial cell interactions as well as neutrophil recruitment to sites of inflammation. Here, we summarise key processes that are dependent upon small GTPases in leukocytes during these early inflammatory events. We place a particular focus on the regulation of integrin-dependent events and their control by Rho and Rap family GTPases as well as their regulators during neutrophil adhesion, chemotaxis and recruitment.
Original languageEnglish
Pages (from-to)649-658
Number of pages10
JournalBiochemical Society Transactions
Volume46
Issue number3
Early online date9 May 2018
DOIs
Publication statusPublished - 19 Jun 2018

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Keywords

  • inflammation
  • integrin
  • neutrophil
  • PI3K
  • small GTPase
  • vascular leakage

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