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Hypoxia induces inflammasome activation and influx of neutrophils and T-cells in the lungs

Fadila Telarevic Cero, Karl Otto Larsen, Geir Christensen, Ole Henning Skjønsberg
European Respiratory Journal 2013 42: P652; DOI:
Fadila Telarevic Cero
Department of Pulmonary Medicine, Oslo University Hospital Ullevål, Oslo, NorwayInstitute for Experimental Medical Research, Oslo University Hospital Ullevål, Oslo, NorwayCenter for Heart Failure Research, University of Oslo, Oslo, Norway
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Karl Otto Larsen
Department of Pulmonary Medicine, Oslo University Hospital Ullevål, Oslo, Norway
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Geir Christensen
Institute for Experimental Medical Research, Oslo University Hospital Ullevål, Oslo, NorwayCenter for Heart Failure Research, University of Oslo, Oslo, Norway
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Ole Henning Skjønsberg
Department of Pulmonary Medicine, Oslo University Hospital Ullevål, Oslo, Norway
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Abstract

Background: Inflammasomes are molecular platforms which are part of the innate immunity and activate IL-18 and IL-1β through caspase-1. They can be activated by microorganisms and physical stress (K. Schroder & J.Tschopp, Cell, 2010). Increased levels of interleukin (IL)-18 have been found during experimental alveolar hypoxia (K.O. Larsen et al. Cardiovasc Res, 2008), but it is not known whether hypoxia activates inflammasomes leading to increased IL-18 and IL-1β levels.

Objectives: To study inflammasome activation and cell infiltration in mouse lungs during hypoxia exposure.

Methods: Lungs were harvested from C57Bl/6j mice at 1-7 days of hypoxia exposure (10%) for histological and Western blot analyses. Active caspase-1, IL-18 and IL-1β were measured.

Results: Histology revealed perivascular infiltration of inflammatory cells and inflammasome components at day 1-7, with neutrophil granulocytes dominating from day 1-3, and T-cells dominating from day 4-7. Active caspase-1 and IL-18 were significantly increased at day 3, 7 and 4 weeks of hypoxia compared to normoxic controls (both p<0.05). IL-1β showed upregulation, but it did not reach statistical significance.

Conclusions: Active Caspase-1 was induced during hypoxia indicating activation of the innate immune system through inflammasomes. Both IL-18 and IL-1β were upregulated, but IL-1β did not reach significance. Activation of the inflammasome may play a role for the inflammatory cell influx and the cytokine mediated progression of lung disease in hypoxic patients.

Acknowledgements: We are grateful to Almira Hasic and Ingeborg Løstegaard Goverud for technical assistance.

  • Animal models
  • Inflammation
  • Lung injury
  • © 2013 ERS
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Hypoxia induces inflammasome activation and influx of neutrophils and T-cells in the lungs
Fadila Telarevic Cero, Karl Otto Larsen, Geir Christensen, Ole Henning Skjønsberg
European Respiratory Journal Sep 2013, 42 (Suppl 57) P652;

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Hypoxia induces inflammasome activation and influx of neutrophils and T-cells in the lungs
Fadila Telarevic Cero, Karl Otto Larsen, Geir Christensen, Ole Henning Skjønsberg
European Respiratory Journal Sep 2013, 42 (Suppl 57) P652;
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