Roles of endothelial cells during infection
Year: 2025
Type: review
Abstract: Endothelial cells (ECs) integrate immune and vascular functions to promote host defense against pathogens. While previously studied as forming passive flow conduits, ECs are now recognized as active contributors to maladaptive inflammation. During acute infection, ECs may promote tissue pathologies, including hypoxia, acidosis, electrolyte disturbances, and capillary barrier breakdown. These pathologies significantly contribute to organ dysfunction and septic shock. In chronic vascular infection, ECs may promote loss of vascular quiescence, contributing to vascular malformations and vaso-occlusive lesions. In this review, we discuss the interplay between the immune and vascular roles of blood ECs, an emerging area of interest with therapeutic implications. While previously overlooked, therapies targeting dysregulation of EC function(s) may show clinical benefit towards improving outcomes related to both acute and chronic forms of infection.
Source: Current Opinion in Immunology
Authors: Zihan Ma, Richard W Pierce, Carrie L Lucas, Clara Abraham, Carlos Fernandez-Hernando, Dan Jane-wit
Institutions: Yale University, VA Connecticut Healthcare System
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $4,410
Funders: U.S. Department of Veterans Affairs, American Federation for Aging Research, American Heart Association, American Society of Transplantation, National Institutes of Health, National Institute of Allergy and Infectious Diseases, National Institute of Diabetes and Digestive and Kidney Diseases
Awards: G151390969, G2463248496, Membrane Attack Complexes, Amyloidosis, and Cardiac Allograft Vasculopathy, Intracellular Membrane Attack Complexes and COVID-19 Immune Hyperactivation, G4730601274, G8815287182, G8994008036, Functional outcomes of inflammatory bowel disease associated variants, Mitochondrial Mechanisms Promoting Innate and Intestinal Immunity
OpenAlex ID: W4413824353
