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The effects of lipopolysaccharide (LPS) on leukocyte migration and macrophage disappearence reaction: role of toll-like receptor 4, MYD88 signaling and nitric oxide production

E Florsheim D Rodriguez; Momtchilo Russo; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)

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

São Paulo 2006

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  • Título:
    The effects of lipopolysaccharide (LPS) on leukocyte migration and macrophage disappearence reaction: role of toll-like receptor 4, MYD88 signaling and nitric oxide production
  • Autor: E Florsheim
  • D Rodriguez; Momtchilo Russo; 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: Introduction: Depending on the dose and route of administration bacterial lipopolysaccharides (LPS), a prototypic Toll-like receptor 4 (TLR4) agonist, can enhance or suppress leukocyte diapedesis and induce a phenomenon known as macrophage disappearance reaction (MDR). Objective: We evaluated the leukocyte influx and MDR in TLR4-normal (C3H/HePas and C57Bl/6), TLR4-deficient (C3H/HeJ) and C57BL/6 MyD88 KO mice. Methods: Mice were injected i.p. with 20 µg of LPS. Total and differential cell counts were determined by hemocytometer and cytospin stained preparations. The standard Griess method was used to quantify NO production. Results: Six hours after LPS injection a discrete influx of neutrophils was detected in TLR4-normal mice. However, the total number of cells, including macrophages, in peritoneal cavity was lower than that of control group (2.23 ± 0.57 x105 versus 7.6 ± 1.2 x105), indicating that peritoneal cells disappeared from peritoneal cavity, or that MDR occurred. Surprisingly, LPS injection in TLR4-deficient mice resulted in a significant influx of neutrophils (5.95 ± 1.6 x105), but MDR was discrete in these animals. In contrast, LPS did not induce neutrophil migration in MyD88KO mice nonetheless the MDR was significant. Finally, significant NO production was detected in all mouse strains except TLR4-deficient. Conclusions: We conclude first that neutrophils influx is MyD88-dependent because it was absent in MyD88KO mice.
    Therefore, our commercial LPS is contaminated with other TLRs ligands that might explain the neutrophil influx in TLR4-deficient mice. Second, MDR is MyD88-independent phenomenon and third, MDR appears to be associated with NO production.
  • Editor: São Paulo
  • Data de criação/publicação: 2006
  • Formato: res. IN.016.
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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