β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32
Summary: American tegumentary leishmaniasis is a vector-borne parasitic disease caused by Leishmania protozoans. Innate immune cells undergo long-term functional reprogramming in response to infection or Bacillus Calmette-Guérin (BCG) vaccination via a process called trained immunity, conferring non...
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Elsevier
2019-09-01
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Series: | Cell Reports |
Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124719310277 |
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Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jéssica Cristina dos Santos Ana Marina Barroso de Figueiredo Muriel Vilela Teodoro Silva Branko Cirovic L. Charlotte J. de Bree Michelle S.M.A. Damen Simone J.C.F.M. Moorlag Rodrigo S. Gomes Monique M. Helsen Marije Oosting Samuel T. Keating A. Schlitzer Mihai G. Netea Fátima Ribeiro-Dias Leo A.B. Joosten |
spellingShingle |
Jéssica Cristina dos Santos Ana Marina Barroso de Figueiredo Muriel Vilela Teodoro Silva Branko Cirovic L. Charlotte J. de Bree Michelle S.M.A. Damen Simone J.C.F.M. Moorlag Rodrigo S. Gomes Monique M. Helsen Marije Oosting Samuel T. Keating A. Schlitzer Mihai G. Netea Fátima Ribeiro-Dias Leo A.B. Joosten β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32 Cell Reports |
author_facet |
Jéssica Cristina dos Santos Ana Marina Barroso de Figueiredo Muriel Vilela Teodoro Silva Branko Cirovic L. Charlotte J. de Bree Michelle S.M.A. Damen Simone J.C.F.M. Moorlag Rodrigo S. Gomes Monique M. Helsen Marije Oosting Samuel T. Keating A. Schlitzer Mihai G. Netea Fátima Ribeiro-Dias Leo A.B. Joosten |
author_sort |
Jéssica Cristina dos Santos |
title |
β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32 |
title_short |
β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32 |
title_full |
β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32 |
title_fullStr |
β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32 |
title_full_unstemmed |
β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32 |
title_sort |
β-glucan-induced trained immunity protects against leishmania braziliensis infection: a crucial role for il-32 |
publisher |
Elsevier |
series |
Cell Reports |
issn |
2211-1247 |
publishDate |
2019-09-01 |
description |
Summary: American tegumentary leishmaniasis is a vector-borne parasitic disease caused by Leishmania protozoans. Innate immune cells undergo long-term functional reprogramming in response to infection or Bacillus Calmette-Guérin (BCG) vaccination via a process called trained immunity, conferring non-specific protection from secondary infections. Here, we demonstrate that monocytes trained with the fungal cell wall component β-glucan confer enhanced protection against infections caused by Leishmania braziliensis through the enhanced production of proinflammatory cytokines. Mechanistically, this augmented immunological response is dependent on increased expression of interleukin 32 (IL-32). Studies performed using a humanized IL-32 transgenic mouse highlight the clinical implications of these findings in vivo. This study represents a definitive characterization of the role of IL-32γ in the trained phenotype induced by β-glucan or BCG, the results of which improve our understanding of the molecular mechanisms governing trained immunity and Leishmania infection control. : dos Santos et al. describe that trained immunity induced by β-glucan confers protection against L. braziliensis infections. Infection control is associated with IL-32 and IL-1 induction. Genetic variation in the IL-32 gene enhances induction of trained immunity leading to proinflammatory gene transcription in bone marrow hematopoietic stem and progenitor cells. Keywords: Leishmania braziliensis, trained immunity, β-glucan, BCG, IL-32, proinflammatory cytokines, IL-32 transgenic mouse |
url |
http://www.sciencedirect.com/science/article/pii/S2211124719310277 |
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doaj-1883448906ac4f4baf4e808ac577a77c2020-11-25T01:27:29ZengElsevierCell Reports2211-12472019-09-01281026592672.e6β-Glucan-Induced Trained Immunity Protects against Leishmania braziliensis Infection: a Crucial Role for IL-32Jéssica Cristina dos Santos0Ana Marina Barroso de Figueiredo1Muriel Vilela Teodoro Silva2Branko Cirovic3L. Charlotte J. de Bree4Michelle S.M.A. Damen5Simone J.C.F.M. Moorlag6Rodrigo S. Gomes7Monique M. Helsen8Marije Oosting9Samuel T. Keating10A. Schlitzer11Mihai G. Netea12Fátima Ribeiro-Dias13Leo A.B. Joosten14Radboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, BrazilInstituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, BrazilInstituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, BrazilMyeloid Cell Biology, Life and Medical Sciences Institute, University of Bonn, 53115 Bonn, GermanyRadboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; Research Center for Vitamins and Vaccines, Bandim Health Project, Statens Serum Institut, Copenhagen, Denmark; Odense Patient Data Explorative Network, University of Southern Denmark and Odense University Hospital, Odense, DenmarkRadboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USARadboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the NetherlandsInstituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, BrazilDepartment of Rheumatology, Radboud University Medical Center, Nijmegen, the NetherlandsRadboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the NetherlandsRadboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the NetherlandsMyeloid Cell Biology, Life and Medical Sciences Institute, University of Bonn, 53115 Bonn, Germany; Single Cell Genomics and Epigenomics Unit at the German Center for Neurodegenerative Diseases and the University of Bonn, 53175 Bonn, GermanyRadboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; Department for Genomics and Immunoregulation, Life and Medical Sciences Institute (LIMES), University of Bonn, GermanyInstituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, Brazil; Corresponding authorRadboud Institute for Molecular Sciences (RILMS), Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, Brazil; Corresponding authorSummary: American tegumentary leishmaniasis is a vector-borne parasitic disease caused by Leishmania protozoans. Innate immune cells undergo long-term functional reprogramming in response to infection or Bacillus Calmette-Guérin (BCG) vaccination via a process called trained immunity, conferring non-specific protection from secondary infections. Here, we demonstrate that monocytes trained with the fungal cell wall component β-glucan confer enhanced protection against infections caused by Leishmania braziliensis through the enhanced production of proinflammatory cytokines. Mechanistically, this augmented immunological response is dependent on increased expression of interleukin 32 (IL-32). Studies performed using a humanized IL-32 transgenic mouse highlight the clinical implications of these findings in vivo. This study represents a definitive characterization of the role of IL-32γ in the trained phenotype induced by β-glucan or BCG, the results of which improve our understanding of the molecular mechanisms governing trained immunity and Leishmania infection control. : dos Santos et al. describe that trained immunity induced by β-glucan confers protection against L. braziliensis infections. Infection control is associated with IL-32 and IL-1 induction. Genetic variation in the IL-32 gene enhances induction of trained immunity leading to proinflammatory gene transcription in bone marrow hematopoietic stem and progenitor cells. Keywords: Leishmania braziliensis, trained immunity, β-glucan, BCG, IL-32, proinflammatory cytokines, IL-32 transgenic mousehttp://www.sciencedirect.com/science/article/pii/S2211124719310277 |