TY - JOUR
T1 - Intracellular communication and immunothrombosis in sepsis
AU - Iba, Toshiaki
AU - Levi, Marcel
AU - Levy, Jerrold H.
N1 - Funding Information: TI has received a research grant from Japan Blood Products Organization and Asahi Kasei Pharmaceuticals. ML has received grants and has participated in advisory boards of NovoNordisk, Eli Lilly, Asahi Kasei Pharmaceuticals America, and Johnson & Johnson. JHL serves on the Steering Committees for Instrumentation Laboratories, Merck, and Octapharma. Publisher Copyright: © 2022 The Authors. Journal of Thrombosis and Haemostasis published by Wiley Periodicals LLC on behalf of International Society on Thrombosis and Haemostasis.
PY - 2022/11
Y1 - 2022/11
N2 - Inflammation and coagulation are the critical responses to infection that include leukocytes, platelets, and vascular endothelial cells responding in concert to eradicate the invading pathogen. In sepsis, a variety of cell surface receptors, including toll-like receptors, Fcγ-receptors, G-protein-coupled receptors, and adhesion receptors, detect the pathogens and elicit thromboinflammatory responses. Concurrently, the molecular patterns released from host damaged cells accelerate the immune responses through binding to the same pattern recognition receptors. Cytokines, chemokines, and extracellular vesicles are important mediators for amplifying the responses to distant cells as part of the systemic response to infections. At the same time, cells communicate with each other via direct contact, adhesion molecules, paracrine mediators, and tunneling nanotubes, which are important for regulating inflammation and thrombus formation. Despite increasing attention to immunothrombosis in sepsis, these close communication systems are less understood but play a critical role in host defense mechanisms. In this review, cellular activation and direct intercellular communication systems in sepsis with a focus on the coagulation response will be considered.
AB - Inflammation and coagulation are the critical responses to infection that include leukocytes, platelets, and vascular endothelial cells responding in concert to eradicate the invading pathogen. In sepsis, a variety of cell surface receptors, including toll-like receptors, Fcγ-receptors, G-protein-coupled receptors, and adhesion receptors, detect the pathogens and elicit thromboinflammatory responses. Concurrently, the molecular patterns released from host damaged cells accelerate the immune responses through binding to the same pattern recognition receptors. Cytokines, chemokines, and extracellular vesicles are important mediators for amplifying the responses to distant cells as part of the systemic response to infections. At the same time, cells communicate with each other via direct contact, adhesion molecules, paracrine mediators, and tunneling nanotubes, which are important for regulating inflammation and thrombus formation. Despite increasing attention to immunothrombosis in sepsis, these close communication systems are less understood but play a critical role in host defense mechanisms. In this review, cellular activation and direct intercellular communication systems in sepsis with a focus on the coagulation response will be considered.
KW - adhesion molecule
KW - endothelial cell
KW - immunothrombosis
KW - platelet
KW - sepsis
KW - thromboinflammation
UR - http://www.scopus.com/inward/record.url?scp=85136689595&partnerID=8YFLogxK
U2 - https://doi.org/10.1111/jth.15852
DO - https://doi.org/10.1111/jth.15852
M3 - Review article
C2 - 35979601
SN - 1538-7933
VL - 20
SP - 2475
EP - 2484
JO - Journal of thrombosis and haemostasis
JF - Journal of thrombosis and haemostasis
IS - 11
ER -