Markus Meissner

Publications (3)5.1 Total impact

• Source

  Available from: Mária A Deli

  Dataset: Lachenmaier J Neuroimmunol 2011

  Sabrina M Lachenmaier, Mária A Deli, Markus Meissner, Oliver Liesenfeld
• Source

  Available from: Oliver Liesenfeld

  Article: Toxoplasma gondii and the blood-brain barrier.

  Sabrina M Feustel, Markus Meissner, Oliver Liesenfeld
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  ABSTRACT: Infection with the protozoan parasite Toxoplasma gondii is characterized by asymptomatic latent infection in the central nervous system and skeletal muscle tissue in the majority of immunocompentent individuals. Life-threatening reactivation of the infection in immunocompromized patients originates from rupture of Toxoplasma cysts in the brain. While major progress has been made in our understanding of the immunopathogenesis of infection the mechanism(s) of neuroinvasion of the parasite remains poorly understood. The present review presents the current understanding of blood-brain barrier (patho)physiology and the interaction of Toxoplasma gondii with cells of the blood-brain barrier.
  Virulence 03/2012; 3(2):182-92. · 2.26 Impact Factor
• Article: Intracellular transport of Toxoplasma gondii through the blood-brain barrier.

  Sabrina M Lachenmaier, Mária A Deli, Markus Meissner, Oliver Liesenfeld
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  ABSTRACT: Toxoplasma gondii establishes latent infection in the central nervous system of immunocompentent hosts. Toxoplasmic encephalitis is a life threatening reactivation of latent infection in the brain of immunocompromised patients. To further understand the mechanisms of entry into the brain of T. gondii we investigated host molecules and cells involved in the passage of the parasite through the blood-brain barrier. First, using microarrays brain endothelial cells were found to upregulate, among others, chemokines and adhesion molecules following infection with tachyzoites. Using flow cytometry we observed upregulated ICAM-1 expression on the surface of brain endothelial cells following infection; ICAM-1 expression was further increased after pre-incubation with IFN-γ. Compared to RH tachyzoites, ME49 tachyzoites induced a stronger upregulation of ICAM-1 and an earlier and stronger IL-6 and MCP-1 secretion by brain endothelial cells. Using an in vitro coculture model of the BBB (primary glia cells and brain endothelial cells) we found a stronger migration of infected antigen-presenting cells compared to lymphocytes (4.63% vs. 0.6% of all cells) across the BBB. Among all antigen-presenting cells CD11b(+)/CD11c(+) cells showed the highest infection rate, whereas the majority of infected cells that migrated through the blood-brain barrier were CD11b(+)/CD11c(-) cells. Infection of PBMCs with type I or type II Toxoplasma strains resulted in similar patterns of cell migration across the in vitro BBB model. In conclusion, these results suggest that T. gondii modulates gene expression of brain endothelial cells to promote its own migration through the blood-brain barrier in a 'Trojan horse' manner. Cells expressing CD11b either with or without CD11c are likely candidate cells for the intracellular transport of T. gondii across the BBB. T. gondii type I and type II strains induced similar migration patterns of antigen-presenting cells across the in vitro BBB.
  Journal of neuroimmunology 11/2010; 232(1-2):119-30. · 2.84 Impact Factor