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Int J Immunopathol Pharmacol. 2017 Dec;30(4):333-340. doi: 10.1177/0394632017734479. Epub 2017 Oct 4.

HSP60 activity on human bronchial epithelial cells.

Author information

1
1 Divisione di Pneumologia e Laboratorio di Citoimmunopatologia dell'Apparato Cardio Respiratorio, Istituti Clinici Scientifici Maugeri SpA SB, IRCCS, Veruno, Italy.
2
2 Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Università degli Studi di Palermo, Palermo, Italy.
3
3 Istituto Euro-Mediterraneo di Scienza e Tecnologia (IEMEST), Palermo, Italy.
4
4 Department of Molecular Medicine, University of Padova, Padova, Italy.
5
5 Department of Microbiology and Immunology, School of Medicine, University of Maryland - Baltimore, Baltimore, MD, USA.
6
6 Institute of Marine and Environmental Technology (IMET), Baltimore, MD, USA.

Abstract

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1-4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (LPS), or cytomix. The cell response was evaluated by measuring the expression of IL-8 and IL-10, respectively, pro- and anti-inflammatory cytokines involved in COPD pathogenesis, as well as of pertinent TLR-4 pathway mediators. Stimulation with HSP60 up-regulated IL-8 at mRNA and protein levels and down-regulated IL-10 mRNA and protein. Likewise, CREB1 mRNA was up-regulated. H2O2 and LPS up-regulated IL-8. Experiments with an inhibitor for p38 showed that this mitogen-activated protein kinase could be involved in the HSP60-mediated pro-inflammatory effects. HSP60 showed pro-inflammatory properties in bronchial epithelial cells mediated by activation of TLR-4-related molecules. The results should prompt further studies on more complex ex-vivo or in-vivo models with the aim to elucidate further the role of those molecules in the pathogenesis of COPD.

KEYWORDS:

16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38α

PMID:
28976240
PMCID:
PMC5806805
DOI:
10.1177/0394632017734479
[Indexed for MEDLINE]
Free PMC Article

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