HSP60 activity on human bronchial epithelial cells

Davide Vallese, Claudia Sangiorgi, Fabio Bucchieri, Angelo Leone, Francesco Cappello, Angelo Leone, Paola Brun, Andrea Giordano, Davide Vallese, Claudia Sangiorgi, Antonino Di Stefano, Isabella Gnemmi, Fabio Bucchieri, Bruno Balbi, Francesco Cappello, Everly Conway De Macario, Alberto J.L. Macario

Risultato della ricerca: Article

4 Citazioni (Scopus)

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.
Lingua originaleEnglish
pagine (da-a)333-340
Numero di pagine8
RivistaDefault journal
Volume30
Stato di pubblicazionePublished - 2017

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Interleukin-8
Human Activities
Chronic Obstructive Pulmonary Disease
Epithelial Cells
Interleukin-10
Messenger RNA
Lipopolysaccharides
Anti-Inflammatory Agents
Chaperonins
Toll-Like Receptors
p38 Mitogen-Activated Protein Kinases
Cultured Cells
Proteins
Chronic Disease
Cytokines

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Pharmacology

Cita questo

HSP60 activity on human bronchial epithelial cells. / Vallese, Davide; Sangiorgi, Claudia; Bucchieri, Fabio; Leone, Angelo; Cappello, Francesco; Leone, Angelo; Brun, Paola; Giordano, Andrea; Vallese, Davide; Sangiorgi, Claudia; Di Stefano, Antonino; Gnemmi, Isabella; Bucchieri, Fabio; Balbi, Bruno; Cappello, Francesco; Conway De Macario, Everly; Macario, Alberto J.L.

In: Default journal, Vol. 30, 2017, pag. 333-340.

Risultato della ricerca: Article

Vallese, D, Sangiorgi, C, Bucchieri, F, Leone, A, Cappello, F, Leone, A, Brun, P, Giordano, A, Vallese, D, Sangiorgi, C, Di Stefano, A, Gnemmi, I, Bucchieri, F, Balbi, B, Cappello, F, Conway De Macario, E & Macario, AJL 2017, 'HSP60 activity on human bronchial epithelial cells', Default journal, vol. 30, pagg. 333-340.
Vallese, Davide ; Sangiorgi, Claudia ; Bucchieri, Fabio ; Leone, Angelo ; Cappello, Francesco ; Leone, Angelo ; Brun, Paola ; Giordano, Andrea ; Vallese, Davide ; Sangiorgi, Claudia ; Di Stefano, Antonino ; Gnemmi, Isabella ; Bucchieri, Fabio ; Balbi, Bruno ; Cappello, Francesco ; Conway De Macario, Everly ; Macario, Alberto J.L. / HSP60 activity on human bronchial epithelial cells. In: Default journal. 2017 ; Vol. 30. pagg. 333-340.
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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.",
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AU - Vallese, Davide

AU - Sangiorgi, Claudia

AU - Bucchieri, Fabio

AU - Leone, Angelo

AU - Cappello, Francesco

AU - Leone, Angelo

AU - Brun, Paola

AU - Giordano, Andrea

AU - Vallese, Davide

AU - Sangiorgi, Claudia

AU - Di Stefano, Antonino

AU - Gnemmi, Isabella

AU - Bucchieri, Fabio

AU - Balbi, Bruno

AU - Cappello, Francesco

AU - Conway De Macario, Everly

AU - Macario, Alberto J.L.

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

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