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Related Experiment Video

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HSP60 activity on human bronchial epithelial cells.

Claudia Sangiorgi1, Davide Vallese1, Isabella Gnemmi1

  • 11 Divisione di Pneumologia e Laboratorio di Citoimmunopatologia dell'Apparato Cardio Respiratorio, Istituti Clinici Scientifici Maugeri SpA SB, IRCCS, Veruno, Italy.

International Journal of Immunopathology and Pharmacology
|October 5, 2017
PubMed
Summary

Heat shock protein 60 (HSP60) exhibits pro-inflammatory effects in bronchial epithelial cells, promoting IL-8 and reducing IL-10. This suggests HSP60

Keywords:
16-HBECOPDCREB1ERK1HSP60IL-10IL-8JNK1MyD88NF-κB p65 subunitTLR-4p38α

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Area of Science:

  • Immunology
  • Cell Biology
  • Respiratory Medicine

Background:

  • Heat shock protein 60 (HSP60) is linked to chronic inflammatory diseases like COPD.
  • Extracellular HSP60's role and mechanisms in inflammation are not fully understood.
  • HSP60 can be secreted and interact with Toll-like receptors (TLRs).

Purpose of the Study:

  • To investigate the pro- or anti-inflammatory effects of HSP60 in human bronchial epithelial cells (16-HBE).
  • To compare HSP60's effects with oxidative, inflammatory, or bacterial challenges.
  • To explore the underlying mechanisms involving TLR-4 and related pathways.

Main Methods:

  • 16-HBE cells were cultured with HSP60, H2O2, LPS, or cytomix for 1-4 hours.
  • Expression of IL-8 (pro-inflammatory) and IL-10 (anti-inflammatory) cytokines was measured at mRNA and protein levels.
  • TLR-4 pathway mediators and CREB1 mRNA were analyzed. p38 MAPK involvement was assessed using an inhibitor.

Main Results:

  • HSP60 stimulation upregulated IL-8 and downregulated IL-10 mRNA and protein.
  • CREB1 mRNA expression was also increased by HSP60.
  • HSP60 demonstrated pro-inflammatory properties, activating TLR-4-related molecules, similar to H2O2 and LPS.

Conclusions:

  • Extracellular HSP60 exhibits pro-inflammatory properties in bronchial epithelial cells.
  • HSP60 activates TLR-4-related pathways, contributing to inflammation.
  • Further in vivo studies are warranted to elucidate HSP60's role in COPD pathogenesis.