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Innate lymphoid cells in isocyanate-induced asthma: role of microRNA-155


Abstract

Background Occupational asthma, induced by workplace exposures to low molecular weight (LMW) agents such as toluene 2,4-diisocyanate (TDI), causes a significant burden to patients and society. Little is known about innate lymphoid cells (ILC) in TDI-induced asthma. A critical regulator of ILC function is microRNA-155, a microRNA associated with asthma.

Objective Determine whether TDI exposure modifies the number of ILC in the lung and whether microRNA-155 contributes to TDI-induced airway inflammation and hyperresponsiveness.

Methods C57BL/6 wild-type and microRNA-155 knockout mice were sensitised and challenged with TDI or vehicle. Intracellular cytokine expression in ILC and T cells was evaluated in bronchoalveolar lavage fluid (BAL) by flow cytometry. Peribronchial eosinophilia and goblet cells were evaluated on lung tissue and airway hyperresponsiveness was measured with the forced oscillation technique. Putative ILC2 cells were identified in bronchial biopsies of subjects with TDI-induced occupational asthma using immunohistochemistry. Human bronchial epithelial cells were exposed to TDI or vehicle.

Results TDI-exposed mice had higher numbers of airway goblet cells, BAL eosinophils, CD4+ T cells and ILC, with a predominant type 2 response and tended to have airway hyperresponsiveness. In TDI-exposed microRNA-155 knockout mice, inflammation and airway hyperresponsiveness was attenuated. TDI exposure induced IL-33 expression in human bronchial epithelial cells and in murine lungs, which was microRNA-155 dependent in mice. GATA3+CD3− cells, presumably ILC2, were present in bronchial biopsies.

Conclusion TDI exposure is associated with increased numbers of ILC. The proinflammatory microRNA-155 is crucial in a murine model of TDI asthma, suggesting its involvement in the pathogenesis of occupational asthma due to LMW agents.

Footnotes

This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.

Conflict of interest: Dr. BLOMME reports grants from Fund for Scientific Research in Flanders , grants from Ghent University, during the conduct of the study.

Conflict of interest: Dr. Provoost has nothing to disclose.

Conflict of interest: Dr. Van Eeckhoutte has nothing to disclose.

Conflict of interest: Mirjam Roffel has nothing to disclose.

Conflict of interest: Dr. Pollaris has nothing to disclose.

Conflict of interest: Annelies Bontinck has nothing to disclose.

Conflict of interest: Dr. Vandenbroucke has nothing to disclose.

Conflict of interest: Dr. Verhamme has nothing to disclose.

Conflict of interest: Dr. JOOS reports grants and personal fees from AstraZeneca, personal fees from Bayer, grants from Chiesi, personal fees from Eureca, grants and personal fees from GlaxoSmithKline, personal fees from Teva, outside the submitted work; all payments were done to his employer.

Conflict of interest: Dr. Cosio has nothing to disclose.

Conflict of interest: Dr. Vanoirbeek has nothing to disclose.

Conflict of interest: Dr. Brusselle has nothing to disclose.

Conflict of interest: Dr. Maes reports grants from Ghent University, grants from Fund for Scientific Research in Flanders, during the conduct of the study; personal fees from GlaxoSmithKline, outside the submitted work; and is shareholder of Oryzon Genomics and of Mendelion Lifesciences SL.

Conflict of interest: Dr. Bazzan has nothing to disclose.

Conflict of interest: Dr. Bonato has nothing to disclose.

Conflict of interest: Dr. Saetta reports grants from Laboratori Guidotti SpA, grants from Chiesi Farmaceutici SpA, outside the submitted work.

  • Received June 28, 2019.
  • Accepted May 10, 2020.

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