Vascular Endothelium and Vector Borne Pathogen Interactions Moez Berrich*,1, Henri-Jean Boulouis1, Martine Monteil1, Claudine Kieda2 and Nadia Haddad*,1
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Current Immunology Reviews, 2012, 8, 227-247 227 Vascular Endothelium and Vector Borne Pathogen Interactions Moez Berrich*,1, Henri-Jean Boulouis1, Martine Monteil1, Claudine Kieda2 and Nadia Haddad*,1 1UPE, Ecole Nationale Vétérinaire d'Alfort, UMR BIPAR, ENVA, ANSES, UPEC, USC INRA, 23, rue du Gl de Gaulle - 94703 Maisons-Alfort, France 2Centre de Biophysique Moléculaire, Centre National de la Recherche Scientifique, Unité Propre de Recherche 4301, 45045 Orléans, France Abstract: The endothelium is the thin layer of cells that lines the lumen of blood and lymphatic vessels. Endothelial cells (ECs) from different locations have distinct and characteristic expression patterns that persist during in vitro culture. Although gene expression patterns in cultured cells clearly reveal the molecular heterogeneity of these ECs, their corelation with their in vivo counterparts remains to be defined. Situated at the interface between blood and tissues, the endothelium plays a central role for critical functions and represents a physical barrier for both blood-borne pathogens and immune cells, which must cross this barrier for trafficking between the bloodstream and tissues. Endothelial cells are target cells for several infectious agents, including Anaplasma, Bartonella, Orientia and Rickettsia. The lack of appropriate spontaneous or experimentally-induced animal models is a serious limitation for the study of pathogen-ECs interactions and is the major justification for the use of ECs cultures. Bartonella adherence to ECs is mediated by type-IV like pili and some outer membrane proteins. Some differences exist among Bartonella species adherence mechanisms. ECs are invaded either by an endocytic uptake or by engulfment of Bartonella. The activation of ECs by chronic inflammation and direct or indirect action of some Bartonella species leads to proliferation, angiogenesis and vasoproliferative tumor growth. Interactions between Anaplasma, Orientia, Rickettsia and ECs are less documented than Bartonella but differ significantly from the mechanisms described for Bartonella. At the least, they do not induce vasoproliferation. This review summarizes our understanding of the diversity of ECs, the vector borne bacterium-ECs interactions and the mechanisms of bacterial virulence and persistence. Keywords: Anaplasma, angiogenesis, apoptosis, Bartonella, endothelial cells, heterogeneity, interactions, macrophages, organ specificity, Orientia, Rickettsia, tumor, vascular endothelium, vector borne bacteria, VEGF. INTRODUCTION Accordingly, in vitro evidence of ECs infection is not sufficient, but can contribute to clarify some pathological The endothelium is a single layer of endothelial cells mechanisms. The lack of appropriate spontaneous or (ECs) that lines the lumen of blood and lymphatic vessels. experimentally-induced animal models is a serious limitation ECs are very heterogeneous and constitute diverse for the study of pathogen-ECs interactions and is the major populations with great differences [1] according to the type justification for the use of ECs cultures. of vessel and the organ they belong to and the biological state [2]. The endothelium is not a passive barrier and plays During infection within hosts the ECs-bacteria important roles in the development and remodeling of interactions result into a broad range of clinical vasculature, maintenance of vascular tone, blood fluidity, manifestations. The list of bacteria that have been found able coagulation, nutrient exchange, homeostasis, angiogenesis, to subvert certain cellular functions, resulting in cell organ development and inflammation [3]. Moreover, ECs invasion, proinflamatory activation and modulation of represent a physical barrier to both blood-borne pathogens apoptosis is limited to some -Proteobacteria (Fig. 1), the and immune cells which must cross this barrier for majority of which belong to the order of Rickettsiales. This trafficking between tissues and the bloodstream. order is composed by two families, the Rickettsiaceae (genus Rickettsia and Orientia) and the Anaplasmataceae (that ECs are target cells for several infectious agents includes the genus Anaplasma, Ehrlichia, Neorickettsia and including some pathogenic bacteria. Valbuena and Walker Wolbachia) [5]. Anaplasma-infected ECs lead to unique [4] have proposed the three following criteria as necessary pathogen-specific host cell functional alterations that are for considering the relationships between pathogenic bacteria likely to be important for pathogen survival, pathogenesis and ECs as significant in the pathological process: Bacteria and human disease induction [6]. Orientia causes vasculitis intracellular location in the ECs of natural hosts; Bacteria in humans by replicating inside macrophages and ECs [7]. must be able to multiply in ECs and the endothelium must be Rickettsiae cause life threatening spotted fevers and typhus a consistent target of the infection during the disease. fevers via bacterial transmission by arthropod inoculation into skin, followed by hematogenous spread and disseminated ECs infection [4]. Some members of another *Address correspondence to this author at the Ecole Nationale Vétérinaire d'Alfort - UMR BIPAR, ENVA, ANSES, UPEC, USC INRA, LERPAZ, 7 family, the Bartonellaceae, not belonging to the Rickettsiales avenue du Général de Gaulle, 94704 Maisons-Alfort, France; order, but closer to the genera Agrobacterium, Brucella, and Tel: 00 33 1 43 96 73 15; Fax: 00 33 1 43 96 71 31; Rhizobium can trigger massive proliferation of ECs, leading E-mails: [email protected]; [email protected] to vascular tumor formation [8-9]. 1875-631X/12 $58.00+.00 © 2012 Bentham Science Publishers 228 Current Immunology Reviews, 2012, Vol. 8, No. 3 Berrich et al. Fig. (1). Different degrees of consequences of intra-cellular infection by bacteria that are able to replicate in ECs. As shown in the figure, the bacteria that are able to induce an anti-apoptotic effect (2) are a fortiori able to induce a persistant bacteremia (1), and the bacteria that are able to induce an angiogenic effect (3) are also able to induce an anti-apoptotic effect. *In various blood cells according to the genus. Understanding the mechanisms that contribute to highly complex topology of the endothelium. The pathogens/endothelium interactions is essential to approach understanding of this complexity improved thanks to the in the processes by which infectious agents penetrate the vitro models of endothelium. Immunohistochemical analyses endothelial barrier and to control the clinical outcome of showed that antigen expression and glycosylation patterns such infectious diseases. are different according to the different organs and tissues where the ECs are originating from [14-20]. This review is dedicated to the study of these interactions and will not consider the sepsis mediated endothelial injury. Bizouarne et al. [21] have demonstrated the fine difference between ECs from the high endothelial ORGAN SPECIFICITY AND HETEROGENEITY OF postcapillary venules (HEV) in peripheral lymph nodes ENDOTHELIAL CELLS (PLN) compared to the cells from the post capillary veinules of the Peyer’s Patches (PP) at the molecular and functional ECs are morphologically and functionally heterogeneous levels. These cells from the HEV in their respective with major differences between those from the macro- versus secondary lymphoid organs, are responsible for the selection micro-circulation as documented for a variety of tissues [10]. of distinct lymphocyte populations. As such, they are They differ morphologically, in size, shape, thickness, regulating the homing process of lymphocytes during the number of microvilli, and position of the nucleus [11] and immune response. Bizouarne et al. [22] and Denis et al. [23] functionally by differences in the released substances and in demonstrated that human ECs from PLN and PP are their interactions with leukocytes and pathogens [12]. responsible for distinct gene expression of adhesion molecules and distinct expression of addressins as well as This heterogeneous population of vascular endothelium distinct endogenous lectin expression and activity. The cells specializes in response to genetic programs and “organo specificity” of the endothelium was proven by environmental factors, which contribute to their ability to Kieda et al. [2] who have established endothelial in vitro play distinct roles in different vessels, tissues, organs, and models representative of the various lymphoid and response to stresses and infection [11]. The endothelium phenotypic diversity reflects the biological needs of the peripheral tissues (Table 1). Moreover, Lamerant and Kieda [24] have used the differential gene expression display to underlying tissue as illustrated by the five distinct ECs types identify endothelial genes that are distinctively expressed and phenotypes of the heart (endocardial, coronary arterial, between those ECs from distinct tissue origin. venous, capillary, and lymphatic). Coronary ECs establish a typical network throughout the myocardium, whereas Several studies support this concept. For example, the endocardial ECs form a large epithelial sheet with no plasma glycoprotein known as von Willebrand factor, is sprouting into the myocardium [13]. prominent in veins, less prominent in arteries, and largely absent from sinusoidal ECs; the endothelial protein C While the cultured ECs became a focal point for research receptor is predominantly expressed by large vessel ECs in vascular biology, increasing evidence