Breaking the wall: targeting of the endothelium by pathogenic bacteria.

INSERM, U895, Toxines Microbiennes dans la Relation Hôte Pathogènes, Centre Méditerranéen de Médecine Moléculaire, C3M, Nice, 06204, Cedex 3, France.
Nature Reviews Microbiology (Impact Factor: 23.32). 02/2010; 8(2):93-104. DOI: 10.1038/nrmicro2269
Source: PubMed

ABSTRACT The endothelium lining blood and lymphatic vessels is a key barrier separating body fluids from host tissues and is a major target of pathogenic bacteria. Endothelial cells are actively involved in host responses to infectious agents, producing inflammatory cytokines, controlling coagulation cascades and regulating leukocyte trafficking. In this Review, a range of bacteria and bacterial toxins are used to illustrate how pathogens establish intimate interactions with endothelial cells, triggering inflammatory responses and coagulation processes and modifying endothelial cell plasma membranes and junctions to adhere to their surfaces and then invade, cross and even disrupt the endothelial barrier.

Download full-text


Available from: Marc Lecuit, Jun 24, 2015
1 Follower
  • Source
    Type I Collagen: Biological Functions, Synthesis and Medicinal Applications, Edited by Maria Eduarda Henriques, Marcio Pinto, 11/2012: chapter 2: pages 45-70; Nova Publishers., ISBN: 978-1-62257-625-8
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Vascular endothelial cells (ECs) form the inner layer of blood vessels and exert crucial functions during immune reactions including coagulation, inflammation, and regulation of innate immunity. Importantly, ECs can interact with T cells in an antigen-specific, i.e., T cell receptor-dependent manner. In this review, we will discuss EC actions and reactions during acute inflammation and focus on the interaction of T cells with ECs at two vascular sites: the high endothelial venule (HEV) of lymph nodes, and the vascular lesion during transplant vasculopathy (TV). HEVs are characterized by a highly active endothelium that produces chemoattracting factors and expresses adhesion molecules to facilitate transit of lymphocytes into the lymph node (LN) parenchyma. Yet, T cell-EC interaction at this anatomical location results neither in T cell activation nor tolerization. In contrast, the endothelium at sites of chronic inflammation, such as solid organ transplants, can promote T cell activation by upregulation of major histocompatibility complex (MHC) and costimulatory molecules. Importantly, a major function of ECs in inflamed tissues must be the maintenance of vascular integrity including the efficient attenuation of effector T cells that may damage the vascular bed. Thus, antigen-specific T cell-EC interaction is characterized by a tightly controlled balance between immunological ignorance, immune activation, and tolerization.
    Frontiers in Immunology 08/2012; 3:279. DOI:10.3389/fimmu.2012.00279
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Staphylococcus aureus, a major causative agent of human infection, produces a large array of virulence factors, including various toxins. Among them, the host RhoA GTPase ADP-ribosylating EDIN toxins are considered as potential virulence factors. Using the polymerase chain reaction (PCR) assay, we analyzed the virulence profile of 256 S. aureus isolates from various clinical sites of infections. We developed specific primers to detect the three isoforms of edin-encoding genes. We found a prevalence of 14% (36 bacteria) of edin-encoding genes among these clinical isolates. Strikingly, we found that 90% of all edin-bearing S. aureus isolates carried the type-C allele. Both the spa types and the profile of virulence factors of these edin-positive isolates are highly variable. Notably, we show for the first time that edin-C-positive isolates were more frequently recovered from deep-seated infections than other types of infections. Our present work, thus, strongly suggests that the presence of edin-C is a risk factor of S. aureus dissemination in tissues and, thus, represents a predictive marker for a pejorative evolution of staphylococcal infections.
    European Journal of Clinical Microbiology 02/2011; 30(8):965-72. DOI:10.1007/s10096-011-1181-6 · 2.54 Impact Factor