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Replication of Brucella melitensis inside primary human monocytes depends on mitogen activated protein kinase

Odyssefs Dimitrakopoulos1, Kassiani Liopeta, George Dimitracopoulos

  • 1University of Patras Medical School, Department of Microbiology, Patras 26500, Greece.

Microbes and Infection
|May 1, 2013
PubMed

Insights

Brucella melitensis evades immune responses by activating Toll-like receptor 2 (TLR2) and mitogen-activated protein kinases (MAPK) in human monocytes. This intricate signaling supports bacterial survival despite initial inflammation.

Area of Science:

  • Immunology
  • Microbiology
  • Cellular Signaling

Background:

  • Brucella infections rely on modulating macrophage immune responses for intracellular survival.
  • The specific signaling pathways enabling Brucella survival in human cells remain incompletely understood.

Purpose of the Study:

  • To investigate the role of Toll-like receptor (TLR)-MAPK signaling pathways in Brucella survival within primary human monocytes.
  • To elucidate the mechanisms by which Brucella melitensis persists inside host cells.

Main Methods:

  • Utilized live clinical strains of Brucella melitensis.
  • Investigated signaling pathways in primary human monocytes.
  • Employed specific MAPK inhibitors (p38, ERK1/2, JNK) and anti-TLR2 blocking antibodies.

Main Results:

  • Brucella melitensis induced a delayed, TLR2-dependent activation of MAPK.
  • Inhibitors and anti-TLR2 antibodies suppressed both pro-inflammatory (TNF-α, IL-6) and anti-inflammatory (IL-10) cytokine production.
  • Intracellular replication of B. melitensis was primarily dependent on p38 and JNK activation, independent of IL-10 levels.

Conclusions:

  • Brucella melitensis survival in human monocytes is critically dependent on the interplay of MAPK family members, activated via TLR2.
  • This survival occurs despite an initial pro-inflammatory immune response, highlighting a complex host-pathogen interaction.

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