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Reduced internalization of TNF-ɑ/TNFR1 down-regulates caspase dependent phagocytosis induced cell death (PICD) in

Stephan Dreschers1, Christian Gille2, Martin Haas1

  • 1Department of Neonatology, University Children's Hospital, Aachen, Germany.

Plos One
|August 10, 2017
PubMed

Insights

Phagocytosis-induced cell death is reduced in cord blood monocytes due to impaired TNF-receptor 1 internalization, potentially prolonging inflammation in newborns.

Area of Science:

  • Immunology
  • Cell Biology
  • Neonatal Research

Background:

  • Phagocytosis-induced cell death (PICD) is crucial for immune homeostasis.
  • Cord blood monocytes (CBMO) exhibit diminished PICD compared to adult monocytes (PBMO), possibly linked to neonatal inflammation.
  • The CD95 pathway's role in PICD differences between CBMO and PBMO is established.

Purpose of the Study:

  • To investigate the hypothesis that TNF-α mediated apoptosis induction is impaired in CBMO due to altered TNFR1 internalization.
  • To compare TNFR1-dependent apoptosis pathways in CBMO and PBMO following Escherichia coli infection.

Main Methods:

  • Monocytes (CBMO and PBMO) were infected with Escherichia coli-GFP.
  • Analysis included monocyte phenotype, phagocytic activity, apoptosis induction, and TNF-α/TNFR expression.
  • Investigated TNFR1 internalization, caspase-8, and caspase-3 activation.

Main Results:

  • CBMO secreted 40% less TNF-α than PBMO during infection.
  • PICD was reduced in CBMO and less responsive to TNF-α neutralization compared to PBMO.
  • CBMO showed reduced TNFR1 internalization and lower caspase-8 activation after E. coli infection or TNF-α stimulation.

Conclusions:

  • TNFR1 internalization is critical for mediating PICD in monocytes post-E. coli infection.
  • Reduced TNFR1 internalization in CBMO contributes to their diminished PICD and potential for sustained inflammation.

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