Mediators of Inflammation

Recruitment of Immune Cells into Inflamed Tissues: Consequences for Endothelial Barrier Integrity and Tissue Functionality


Status
Published

Lead Editor

1Cinvestav-IPN, Mexico City, Mexico

2Tufts University, Boston, USA

3William Harvey Research Institute, London, UK

4Sanquin Research Center, Amsterdam, Netherlands


Recruitment of Immune Cells into Inflamed Tissues: Consequences for Endothelial Barrier Integrity and Tissue Functionality

Description

Immune cell trafficking is a vital process of immune surveillance and proper immune responses to tissue injury or invading pathogens. Transmigrated leukocytes contribute to pathogen clearance and resolution of inflammation and are thus indispensable for tissue health. However, uncontrolled extravasation may provoke excessive release of proinflammatory cytokines, proteases, and reactive oxygen species that can induce endothelial dysfunction and tissue damage in various pathological inflammatory conditions including sepsis, autoimmune, and cardiovascular diseases. The leukocyte extravasation cascade requires expression/activation of adhesion receptors, coordinated activation of signalling pathways and cytoskeletal remodelling in all cell types involved. In vitroand in vivo data indicate that overactivated leukocytes are capable of inflicting considerable endothelial injury with increased permeability eventually causing tissue damage and organ failure. The complex nature of physiological and pathological leukocyte extravasation leaves investigators with many open questions regarding the mechanisms that control leukocyte-endothelial interaction during the extravasation cascade to ensure appropriate immune responses.

The purpose of this special issue is to publish high-quality original research papers as well as review articles addressing recent conceptual and/or methodological advances in the field of leukocyte extravasation and endothelial dysfunction during inflammatory diseases. Original articles are encouraged explaining mechanisms by which aberrant leukocyte responses cause endothelial barrier dysfunction and organ failure. Review articles are encouraged discussing questions that have recently been answered and problems that remain to be solved in the field of inflammatory immune cell recruitment.

Potential topics include, but are not limited to:

  • Leukocyte-endothelial receptor-ligand interactions
  • Endothelial regulation of T cell subset recruitment
  • Signal transduction pathways regulating the leukocyte extravasation cascade
  • Cytokine/chemokine-dependent microenvironmental priming of leukocytes
  • Mechanisms of leukocyte-induced endothelial hyperpermeability
  • Role of excessive leukocyte recruitment in organ failure during systemic inflammations
  • Leukocyte traffic in inflammatory diseases including autoimmune and cardiovascular diseases
  • Leukocyte-induced endothelial-mesenchymal transition and fibrosis
  • Actin dynamics in leukocytes and endothelial cells allowing the required morphological changes
  • Mechanisms determining the route of transmigration: trans- versus paracellular
  • Breaking barriers: how leukocytes cross the endothelium, pericytes, and basement membrane
  • Epidemiologic studies on inflammatory diseases caused by excessive leukocyte recruitment
  • Novel in vivo and in vitro models to study leukocyte-endothelial interactions
  • New methodological approaches to monitor immune cell traffic
Mediators of Inflammation
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Acceptance rate14%
Submission to final decision136 days
Acceptance to publication27 days
CiteScore7.700
Journal Citation Indicator0.570
Impact Factor4.6
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