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TRL2-dependent PI3-kinase pathway contributes to mycobacteria-induced cytoskeletal rearrangements essential for macrophage motility

Elena B Lasunskaia Mariana N N Campos; Marcelle R M de Andrade; Renato A Da Matta; Thereza Liberman Kipnis; Marcelo Einicker-Lamas; Wilmar Dias da Silva; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)

Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006

São Paulo 2006

Item não circula. Consulte sua biblioteca.(Acessar)

  • Título:
    TRL2-dependent PI3-kinase pathway contributes to mycobacteria-induced cytoskeletal rearrangements essential for macrophage motility
  • Autor: Elena B Lasunskaia
  • Mariana N N Campos; Marcelle R M de Andrade; Renato A Da Matta; Thereza Liberman Kipnis; Marcelo Einicker-Lamas; Wilmar Dias da Silva; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)
  • Assuntos: IMUNOLOGIA
  • É parte de: Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006
  • Notas: Disponível em CD-ROM
  • Descrição: Macrophage migration and adhesion are important for the control of mycobacterial infection and are critically dependent on the reorganization of the cytoskeleton. Mycobacteria elicit rapid morphological changes such as cell spreading a process relevant to in vivo changes of macrophage shape during extravasation and migration. In this study we investigated the BCG mycobacteria-induced signaling events leading to macrophage cytoskeletal rearrangements employing specific pharmacological inhibitors to suppress distinct kinase pathways known to be elicited by infection. Viable or lysed mycobacteria, as well as purified cell wall lipoprotein p19, TLR2 agonist, induced RAW264.7 cells to extend actin-rich pseudopods which impart radial spreading within 3 h leading later to persistent cell polarization. BCG induced rapid activation of phosphatidylinositol 3- kinase, PI3K, activation which was recruited to the activated TLR2 receptor. TLR2- neutralizing antibody inhibited macrophage spreading and PI3K activation induced by p19. Additionally, BCG failed to induce spreading and polarization in bone marrow-derived macrophages from TLR2- knock-out mice in contrast to their TLR2- expressing counterparts. Neither MEK1/ERK, p38 MAPK nor NF-kB activation were important for the early cytoskeletal rearrangements observed although suppression of these pathways is known to inhibit chemokine secretion by activated macrophages. B2-integrins blockade with a
    corresponding antibody inhibited macrophage spreading and polarization but had no effect on pseudopodia protrusions demonstrating the down-stream position of integrin-mediated adhesion in PI3K- dependent signaling pathway leading to motility phenotype. The obtained data demonstrate that the direct effect of mycobacteria on macrophage shape might be mediated through TLR2-dependent PI3K activation.
  • Editor: São Paulo
  • Data de criação/publicação: 2006
  • Formato: res. CI.009.
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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