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Extracellular Matrix Oxidised by the Granulocyte Oxidants Hypochlorous and Hypobromous Acid Reduces Lung Fibroblast Adhesion and Proliferation In Vitro.
Papanicolaou, Michael; He, Patrick; Rutting, Sandra; Ammit, Alaina; Xenaki, Dikaia; van Reyk, David; Oliver, Brian G.
Afiliação
  • Papanicolaou M; Faculty of Science, School of Life Sciences, University of Technology Sydney, Sydney, NSW 2007, Australia.
  • He P; Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia.
  • Rutting S; Faculty of Science, School of Life Sciences, University of Technology Sydney, Sydney, NSW 2007, Australia.
  • Ammit A; Woolcock Emphysema Centre, Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW 2037, Australia.
  • Xenaki D; Woolcock Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, The University of Sydney, Sydney, NSW 2037, Australia.
  • van Reyk D; Faculty of Science, School of Life Sciences, University of Technology Sydney, Sydney, NSW 2007, Australia.
  • Oliver BG; Woolcock Emphysema Centre, Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW 2037, Australia.
Cells ; 10(12)2021 11 29.
Article em En | MEDLINE | ID: mdl-34943857
ABSTRACT
Chronic airway inflammation and oxidative stress play crucial roles in the pathogenesis of chronic inflammatory lung diseases, with airway inflammation being a key driving mechanism of oxidative stress in the lungs. Inflammatory responses in the lungs activate neutrophils and/or eosinophils, leading to the generation of hypohalous acids (HOX). These HOX oxidants can damage the extracellular matrix (ECM) structure and may influence cell-ECM interactions. The ECM of the lung provides structural, mechanical, and biochemical support for cells and determines the airway structure. One of the critical cells in chronic respiratory disease is the fibroblast. Thus, we hypothesised that primary human lung fibroblasts (PHLF) exposed to an oxidised cell-derived ECM will result in functional changes to the PHLF. Here, we show that PHLF adhesion, proliferation, and inflammatory cytokine secretion is affected by exposure to HOX-induced oxidisation of the cell-derived ECM. Furthermore, we investigated the impact on fibroblast function from the presence of haloamines in the ECM. Haloamines are chemical by-products of HOX and, like the HOX, haloamines can also modify the ECM. In conclusion, this study revealed that oxidising the cell-derived ECM might contribute to functional changes in PHLF, a key mechanism behind the pathogenesis of inflammatory lung diseases.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Bromatos / Oxidantes / Ácido Hipocloroso / Matriz Extracelular / Fibroblastos / Granulócitos / Pulmão Limite: Humans / Middle aged Idioma: En Revista: Cells Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Austrália

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Bromatos / Oxidantes / Ácido Hipocloroso / Matriz Extracelular / Fibroblastos / Granulócitos / Pulmão Limite: Humans / Middle aged Idioma: En Revista: Cells Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Austrália