Platelets promote Brucella abortus monocyte invasion by establishing complexes with monocytes

Autor: Lis N. Velásquez, M. Ayelén Milillo, M. Victoria Delpino, Ana M. Rodríguez, Roberto Gabriel Pozner, Paula Barrionuevo, Verónica I Landoni, Guillermo H. Giambartolomei, Aldana Trotta
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
THP-1 Cells
BRUCELLA ABORTUS
Brucella abortus
Cell Communication
030204 cardiovascular system & hematology
Monocytes
Thromboxane A2
chemistry.chemical_compound
0302 clinical medicine
Immunology and Allergy
Platelet
Cells
Cultured

Chemokine CCL2
Original Research
complexes
purl.org/becyt/ford/3.1 [https]
CD56 Antigen
PLATELETS
Interleukin-10
Interleukin 10
Medicina Básica
medicine.anatomical_structure
monocytes/macrophages
brucellosis
platelets
purl.org/becyt/ford/3 [https]
COMPLEXES
lcsh:Immunologic diseases. Allergy
early infection
Blood Platelets
CIENCIAS MÉDICAS Y DE LA SALUD
Immunology
Inmunología
Microbiology
Cell Line
03 medical and health sciences
medicine
Humans
Interleukin 8
Platelet activation
EARLY INFECTION
BRUCELLOSIS
Tumor Necrosis Factor-alpha
Monocyte
Interleukin-8
MONOCYTES/MACROPHAGES
Fibrinogen binding
030104 developmental biology
chemistry
lcsh:RC581-607
Platelet factor 4
Zdroj: CONICET Digital (CONICET)
Consejo Nacional de Investigaciones Científicas y Técnicas
instacron:CONICET
Frontiers in Immunology
Frontiers in Immunology, Vol 9 (2018)
DOI: 10.3389/fimmu.2018.01000/full
Popis: Brucellosis is an infectious disease elicited by bacteria of the genus Brucella. Platelets have been extensively described as mediators of hemostasis and responsible for maintaining vascular integrity. Nevertheless, they have been recently involved in the modulation of innate and adaptive immune responses. Although many interactions have been described between Brucella abortus and monocytes/macrophages, the role of platelets during monocyte/macrophage infection by these bacteria remained unknown. The aim of this study was to investigate the role of platelets in the immune response against B. abortus. We first focused on the possible interactions between B. abortus and platelets. Bacteria were able to directly interact with platelets. Moreover, this interaction triggered platelet activation, measured as fibrinogen binding and P-selectin expression. We further investigated whether platelets were involved in Brucella-mediated monocyte/macrophage early infection. The presence of platelets promoted the invasion of monocytes/macrophages by B. abortus. Moreover, platelets established complexes with infected monocytes/macrophages as a result of a carrier function elicited by platelets. We also evaluated the ability of platelets to modulate functional aspects of monocytes in the context of the infection. The presence of platelets during monocyte infection enhanced IL-1β, TNF-α, IL-8, and MCP-1 secretion while it inhibited the secretion of IL-10. At the same time, platelets increased the expression of CD54 (ICAM-1) and CD40. Furthermore, we showed that soluble factors released by B. abortus-activated platelets, such as soluble CD40L, platelet factor 4, platelet-activating factor, and thromboxane A2, were involved in CD54 induction. Overall, our results indicate that platelets can directly sense and react to B. abortus presence and modulate B. abortus-mediated infection of monocytes/macrophages increasing their pro-inflammatory capacity, which could promote the resolution of the infection. Fil: Trotta, Aldana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Velasquez, Lis Noelia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Milillo, María Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Rodríguez, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Landoni, Verónica Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Giambartolomei, Guillermo Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Pozner, Roberto Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Barrionuevo, Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Databáze: OpenAIRE