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Pneumocystis-mediated IL-8 release by macrophages requires coexpression of mannose receptors and TLR2

Souvenir D Tachado1, Jianmin Zhang, Jinping Zhu

  • 1Division of Pulmoary, Critical Care and Sleep Medicine, Department of Medicine, Kirstein Hall, Room E/KSB-23, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.

Journal of Leukocyte Biology
|October 6, 2006
PubMed

Insights

Pneumocystis (Pc) fungal infection triggers IL-8 release from human alveolar macrophages (AM). This requires both the mannose receptor (MR) and Toll-like receptor 2 (TLR2) to be present and interact, highlighting combinatorial innate immunity.

Area of Science:

  • Immunology
  • Infectious Disease
  • Cell Biology

Background:

  • Pneumocystis (Pc) fungal infection stimulates IL-8 release from human alveolar macrophages (AM).
  • The specific receptors mediating this IL-8 release in response to Pc are not fully understood.
  • Toll-like receptor 2 (TLR2) recognizes fungal components, but its role in Pc-induced signaling is unknown.

Purpose of the Study:

  • To identify the receptors responsible for Pneumocystis (Pc)-induced IL-8 release by human alveolar macrophages (AM).
  • To investigate the role of Toll-like receptor 2 (TLR2) and mannose receptor (MR) in this immune response.
  • To elucidate the signaling pathways involved in Pc-mediated IL-8 production.

Main Methods:

  • Human AM were stimulated with Pc, and IL-8 release was measured.
  • Neutralizing antibodies against TLR2 and gene silencing of MR were employed.
  • HEK293 cells were transfected with TLR2 and/or MR cDNA for functional assays.
  • Protein interactions, transcription factor activation (NF-kappaB), and MAPK pathways (ERK1/2, JNK) were analyzed.

Main Results:

  • Pc induced IL-8 release in human AM, which was reduced by anti-TLR2 antibody and MR gene silencing.
  • HEK293 cells required co-expression of both TLR2 and MR to release IL-8 upon Pc stimulation.
  • Pc promoted direct interaction between MR and TLR2 on human AM, and IL-8 release involved NF-kappaB and MAPKs.

Conclusions:

  • Co-expression and interaction of mannose receptor (MR) and Toll-like receptor 2 (TLR2) are essential for Pneumocystis (Pc)-mediated IL-8 release by human alveolar macrophages (AM).
  • Combinatorial engagement of innate immune receptors provides specificity to macrophage responses against fungal pathogens.
  • This study clarifies the molecular mechanisms underlying innate immune recognition of Pneumocystis.

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