title: Bacteria and endothelial cells: a toxic relationship.
abstract: Pathogenic bacteria use the bloodstream as a highway for getting around the body, and thus have to find ways to enter and exit through the endothelium. Many bacteria approach this problem by producing toxins that can breach the endothelial barrier through diverse creative mechanisms, including directly killing endothelial cells (ECs), weakening the cytoskeleton within ECs, and breaking the junctions between ECs. Toxins can also modulate the immune response by influencing endothelial biology, and can modulate endothelial function by influencing the response of leukocytes. Understanding these interactions, in both the in vitro and in vivo contexts, is of critical importance for designing new therapies for sepsis and other severe bacterial diseases.
authors.affiliation: Department of Microbiology, New York University School of Medicine, New York, NY 10016, United States.
authors.forename: Ashira
authors.initials: A
authors.lastname: Lubkin
authors.affiliation: Department of Microbiology, New York University School of Medicine, New York, NY 10016, United States. Electronic address: victor.torres@nyumc.org.
authors.forename: Victor J
authors.initials: VJ
authors.lastname: Torres
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology / Q000382:microbiology* / Q000503:physiopathology*; D001427:Bacterial Toxins / Q000378:metabolism; D022162:Cytoplasmic Vesicles / Q000382:microbiology; D042783:Endothelial Cells / Q000382:microbiology* / Q000473:pathology*; D004730:Endothelium, Vascular / Q000382:microbiology; D006090:Gram-Negative Bacteria / Q000472:pathogenicity*; D006801:Humans; D051379:Mice; D018805:Sepsis / Q000382:microbiology; D013211:Staphylococcus aureus / Q000472:pathogenicity
chemical_list: D001427:Bacterial Toxins