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

摘要: Immune cell trafficking is critical for survival. In order to fulfil their functions in surveillance and immune responses, leukocytes need exit the blood stream reach sites of infection or injury peripheral tissues [1]. Once transmigrated, trigger pathogen clearance, resolution inflammation, wound healing. On other hand, excessive extravasation leukocytes, as seen pathological inflammatory conditions including sepsis, autoimmune, cardiovascular diseases, can provoke tissue damage due release proinflammatory cytokines, chemokines, reactive oxygen species. These substances cause endothelial overactivation triggering leukocyte transmigration dysfunction [2]. The complex nature physiological makes it tricky define a threshold where beneficial ends detrimental starts. Thus, utmost importance better understand mechanisms that control leukocyte-endothelial interactions during cascade behaviour within ensure appropriate responses. purpose this special issue was publish original research review articles addressing recent conceptual advances field recruitment, dysfunction, inflammation. The editors contributed article which they highlight certain different subsets exploit achieve goal transmigration. This actually very important when comes treatment diseases caused by subset. case, desired only interfere with subset without affecting others avoid complete suppression would severe side effects. Such include tyrosine phosphorylation adhesion receptors are summarized Dr. A. P. Adam. He highlights signalling pathways downstream cytokines adhering induce junctional proteins such VE-cadherin. discusses consequences these phosphorylations may not lead junction disassembly J. Kryczka Boncela nicely multidimensional impact skin fibrosis emphasizing current knowledge about recruitment types wounded enclosure. A fine balance between scar formation massive required while promoting M. C. Souza colleagues present comprehensive on cerebral malaria. authors summarize known brain lung endothelium challenges using experimental malaria data animals interpret human Moreover, Millan group how once extravasated, interact polarized epithelial cells inflamed tissues. They emphasize secrete chemokines asymmetrically, but also polarize guide across monolayers. Cedervall latest findings alterations vascular tumor tumor-associated summarized. discuss circulating tumor-derived factors drive systemic inflammation vasculature distant organs. In clinical study, Lukasz elegantly showed plasma angiopoietin-2 levels have predictive value complicated course hemolytic uremic syndrome. Using vitro, serum from patients reduced barrier stability. S. Denk coworkers diagnostic implications presence JAM-1 circulation detection polytrauma. Kirchhoff developed method potentially help identifying traumatic infarction showing monocytes accumulate shortly after onset infarct. another article, E. Gallego-Colon demonstrate number infiltrating decreased heart myocardial whereas anti-inflammatory macrophages increased mice overexpressing insulin-like growth factor-1Ea (IGF-1Ea) leading cardiac functional recovery. pro- repair infarction, part controlled IGF-1Ea. Dorosz provide new evidence IL-27 promotes signals downregulated damage-associated molecular pattern molecule calprotectin through involving STAT-1. modulator early dysfunction. We hope will be clinicians researchers those working acute chronic diseases. studies published insights into physiologically relevant hopefully stimulate development novel ideas therapeutic strategies.