Myeloid cell deficiency of p38γ/p38δ protects against candidiasis and regulates antifungal immunity
Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate imm...
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| Published in | EMBO molecular medicine Vol. 10; no. 5; pp. 1 - n/a |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.05.2018
EMBO Press John Wiley and Sons Inc Springer Nature |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1757-4676 1757-4684 1757-4684 |
| DOI | 10.15252/emmm.201708485 |
Cover
| Abstract | Candida albicans
is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to
C. albicans
. We describe a new TAK1‐TPL2‐MKK1‐ERK1/2 pathway in macrophages, which is activated by Dectin‐1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against
C. albicans
infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper‐inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ‐null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating
C. albicans
infection in humans.
Synopsis
Candida albicans
infections cause high mortality in immunocompromised patients. This study shows that p38γ/p38δ are essential for the immune response to
C. albicans
by regulating host antifungal activity. p38γ/p38δ inhibition reduces mice fungal burden, establishing p38γ/p38δ as therapeutic targets.
Deletion of p38γ/p38δ protects mice from
C. albicans
infection.
p38γ/p38δ control fungicidal capacity through ROS and iNOS production.
p38γ/p38δ regulate the inflammatory response to
C. albicans
through a new Dectin‐1 pathway in macrophages.
Chemical inhibition of p38γ/p38δ reduces fungal burden in a candidiasis mouse model.
Graphical Abstract
Candida albicans
infections cause high mortality in immunocompromised patients. This study shows that p38γ/p38δ are essential for the immune response to
C. albicans
by regulating host antifungal activity. p38γ/p38δ inhibition reduces mice fungal burden, establishing p38γ/p38δ as therapeutic targets. |
|---|---|
| AbstractList | Candida albicans
is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to
C. albicans
. We describe a new TAK1‐TPL2‐MKK1‐ERK1/2 pathway in macrophages, which is activated by Dectin‐1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against
C. albicans
infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper‐inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ‐null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating
C. albicans
infection in humans.
Synopsis
Candida albicans
infections cause high mortality in immunocompromised patients. This study shows that p38γ/p38δ are essential for the immune response to
C. albicans
by regulating host antifungal activity. p38γ/p38δ inhibition reduces mice fungal burden, establishing p38γ/p38δ as therapeutic targets.
Deletion of p38γ/p38δ protects mice from
C. albicans
infection.
p38γ/p38δ control fungicidal capacity through ROS and iNOS production.
p38γ/p38δ regulate the inflammatory response to
C. albicans
through a new Dectin‐1 pathway in macrophages.
Chemical inhibition of p38γ/p38δ reduces fungal burden in a candidiasis mouse model.
Graphical Abstract
Candida albicans
infections cause high mortality in immunocompromised patients. This study shows that p38γ/p38δ are essential for the immune response to
C. albicans
by regulating host antifungal activity. p38γ/p38δ inhibition reduces mice fungal burden, establishing p38γ/p38δ as therapeutic targets. Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to C. albicans We describe a new TAK1-TPL2-MKK1-ERK1/2 pathway in macrophages, which is activated by Dectin-1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against C. albicans infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper-inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ-null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating C. albicans infection in humans.Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to C. albicans We describe a new TAK1-TPL2-MKK1-ERK1/2 pathway in macrophages, which is activated by Dectin-1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against C. albicans infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper-inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ-null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating C. albicans infection in humans. Abstract Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to C. albicans. We describe a new TAK1‐TPL2‐MKK1‐ERK1/2 pathway in macrophages, which is activated by Dectin‐1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against C. albicans infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper‐inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ‐null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating C. albicans infection in humans. is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to We describe a new TAK1-TPL2-MKK1-ERK1/2 pathway in macrophages, which is activated by Dectin-1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper-inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ-null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating infection in humans. Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to C. albicans. We describe a new TAK1‐TPL2‐MKK1‐ERK1/2 pathway in macrophages, which is activated by Dectin‐1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against C. albicans infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper‐inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ‐null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating C. albicans infection in humans. Synopsis Candida albicans infections cause high mortality in immunocompromised patients. This study shows that p38γ/p38δ are essential for the immune response to C. albicans by regulating host antifungal activity. p38γ/p38δ inhibition reduces mice fungal burden, establishing p38γ/p38δ as therapeutic targets. Deletion of p38γ/p38δ protects mice from C. albicans infection. p38γ/p38δ control fungicidal capacity through ROS and iNOS production. p38γ/p38δ regulate the inflammatory response to C. albicans through a new Dectin‐1 pathway in macrophages. Chemical inhibition of p38γ/p38δ reduces fungal burden in a candidiasis mouse model. Candida albicans infections cause high mortality in immunocompromised patients. This study shows that p38γ/p38δ are essential for the immune response to C. albicans by regulating host antifungal activity. p38γ/p38δ inhibition reduces mice fungal burden, establishing p38γ/p38δ as therapeutic targets. Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to C. albicans . We describe a new TAK 1‐ TPL 2‐ MKK 1‐ ERK 1/2 pathway in macrophages, which is activated by Dectin‐1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against C. albicans infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper‐inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ‐null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38 MAPK s may be therapeutic targets for treating C. albicans infection in humans. Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need due to the low efficiency and resistance to current antifungal drugs. Here, we show that p38γ and p38δ regulate the innate immune response to C. albicans. We describe a new TAK1‐TPL2‐MKK1‐ERK1/2 pathway in macrophages, which is activated by Dectin‐1 engagement and positively regulated by p38γ/p38δ. In mice, p38γ/p38δ deficiency protects against C. albicans infection by increasing ROS and iNOS production and thus the antifungal capacity of neutrophils and macrophages, and by decreasing the hyper‐inflammation that leads to severe host damage. Leucocyte recruitment to infected kidneys and production of inflammatory mediators are decreased in p38γ/δ‐null mice, reducing septic shock. p38γ/p38δ in myeloid cells are critical for this effect. Moreover, pharmacological inhibition of p38γ/p38δ in mice reduces fungal burden, revealing that these p38MAPKs may be therapeutic targets for treating C. albicans infection in humans. |
| Author | González‐Romero, Diego Netea, Mihai G Shpiro, Natalia Dominguez‐Andrés, Jorge Brown, Gordon D Zur, Rafal Aparicio, Noelia Sanz‐Ezquerro, Juan J Alsina‐Beauchamp, Dayanira Risco, Ana Cuenda, Ana Ardavín, Carlos Martín‐Serrano, Miguel A Escós, Alejandra Fajardo, Pilar Díaz‐Mora, Ester Alemany, Susana del Fresno, Carlos |
| AuthorAffiliation | 2 Immunobiology of Inflammation Laboratory Centro Nacional de Investigaciones Cardiovasculares Carlos III Madrid Spain 3 Medical Research Council Protein Phosphorylation Unit Sir James Black Building School of Life Sciences University of Dundee Dundee UK 7 Department of Cellular and Molecular Biology CNB/CSIC Madrid Spain 1 Department of Immunology and Oncology Centro Nacional de Biotecnología/CSIC Madrid Spain 6 Instituto de Investigaciones Biomédicas Alberto Sols CSIC‐UAM Madrid Spain 4 Aberdeen Fungal Group Institute of Medical Sciences Medical Research Council Centre for Medical Mycology at the University of Aberdeen Aberdeen UK 5 Department of Internal Medicine and Radboud Center for Infectious Diseases Radboud University Nijmegen Medical Centre Nijmegen The Netherlands |
| AuthorAffiliation_xml | – name: 4 Aberdeen Fungal Group Institute of Medical Sciences Medical Research Council Centre for Medical Mycology at the University of Aberdeen Aberdeen UK – name: 5 Department of Internal Medicine and Radboud Center for Infectious Diseases Radboud University Nijmegen Medical Centre Nijmegen The Netherlands – name: 3 Medical Research Council Protein Phosphorylation Unit Sir James Black Building School of Life Sciences University of Dundee Dundee UK – name: 1 Department of Immunology and Oncology Centro Nacional de Biotecnología/CSIC Madrid Spain – name: 2 Immunobiology of Inflammation Laboratory Centro Nacional de Investigaciones Cardiovasculares Carlos III Madrid Spain – name: 6 Instituto de Investigaciones Biomédicas Alberto Sols CSIC‐UAM Madrid Spain – name: 7 Department of Cellular and Molecular Biology CNB/CSIC Madrid Spain |
| Author_xml | – sequence: 1 givenname: Dayanira surname: Alsina‐Beauchamp fullname: Alsina‐Beauchamp, Dayanira organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 2 givenname: Alejandra orcidid: 0000-0002-2990-7920 surname: Escós fullname: Escós, Alejandra organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 3 givenname: Pilar surname: Fajardo fullname: Fajardo, Pilar organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 4 givenname: Diego surname: González‐Romero fullname: González‐Romero, Diego organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 5 givenname: Ester surname: Díaz‐Mora fullname: Díaz‐Mora, Ester organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 6 givenname: Ana surname: Risco fullname: Risco, Ana organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 7 givenname: Miguel A surname: Martín‐Serrano fullname: Martín‐Serrano, Miguel A organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 8 givenname: Carlos surname: del Fresno fullname: del Fresno, Carlos organization: Immunobiology of Inflammation Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III – sequence: 9 givenname: Jorge surname: Dominguez‐Andrés fullname: Dominguez‐Andrés, Jorge organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 10 givenname: Noelia surname: Aparicio fullname: Aparicio, Noelia organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 11 givenname: Rafal surname: Zur fullname: Zur, Rafal organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 12 givenname: Natalia surname: Shpiro fullname: Shpiro, Natalia organization: Medical Research Council Protein Phosphorylation Unit, Sir James Black Building, School of Life Sciences, University of Dundee – sequence: 13 givenname: Gordon D surname: Brown fullname: Brown, Gordon D organization: Aberdeen Fungal Group, Institute of Medical Sciences, Medical Research Council Centre for Medical Mycology at the University of Aberdeen – sequence: 14 givenname: Carlos surname: Ardavín fullname: Ardavín, Carlos organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC – sequence: 15 givenname: Mihai G surname: Netea fullname: Netea, Mihai G organization: Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Nijmegen Medical Centre – sequence: 16 givenname: Susana surname: Alemany fullname: Alemany, Susana organization: Instituto de Investigaciones Biomédicas Alberto Sols, CSIC‐UAM – sequence: 17 givenname: Juan J surname: Sanz‐Ezquerro fullname: Sanz‐Ezquerro, Juan J organization: Department of Cellular and Molecular Biology, CNB/CSIC – sequence: 18 givenname: Ana orcidid: 0000-0002-9013-5077 surname: Cuenda fullname: Cuenda, Ana email: acuenda@cnb.csic.es organization: Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29661910$$D View this record in MEDLINE/PubMed |
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| Keywords | kinase inhibitor infection p38MAPK signalling Candida albicans |
| Language | English |
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| References | 2011; 434 2017; 42 2010; 10 2012; 122 2013; 208 2013; 123 1999; 163 2004; 5 2008; 6 2010; 140 2007; 76 2014; 66 2012; 845 2003; 197 2002; 49 2014; 127 2013; 13 2015; 373 2003; 3 2011; 21 2008; 20 2009; 19 2007; 219 2010; 7 2014; 10 2015; 15 2005; 192 2015; 6 2009; 21 2006; 12 2004; 382 2016; 54 2013; 344 2007; 50 2008; 11 2007; 408 2014; 111 2012; 32 2012; 109 2016; 4 2005; 280 2009; 9 2009; 8 2016; 374 2014; 74 2012; 7 2012; 4 2003; 21 2012; 8 e_1_2_9_31_1 e_1_2_9_52_1 e_1_2_9_50_1 Kullberg BJ (e_1_2_9_24_1) 2016; 374 e_1_2_9_10_1 e_1_2_9_35_1 e_1_2_9_12_1 e_1_2_9_33_1 e_1_2_9_14_1 e_1_2_9_39_1 e_1_2_9_16_1 e_1_2_9_37_1 e_1_2_9_18_1 e_1_2_9_41_1 e_1_2_9_20_1 e_1_2_9_22_1 e_1_2_9_45_1 e_1_2_9_43_1 e_1_2_9_8_1 e_1_2_9_6_1 e_1_2_9_4_1 e_1_2_9_2_1 e_1_2_9_26_1 e_1_2_9_49_1 e_1_2_9_28_1 e_1_2_9_47_1 e_1_2_9_51_1 e_1_2_9_11_1 e_1_2_9_34_1 e_1_2_9_13_1 e_1_2_9_32_1 Netea MG (e_1_2_9_30_1) 1999; 163 e_1_2_9_15_1 e_1_2_9_38_1 e_1_2_9_17_1 e_1_2_9_36_1 e_1_2_9_19_1 e_1_2_9_42_1 e_1_2_9_40_1 e_1_2_9_21_1 e_1_2_9_46_1 e_1_2_9_23_1 e_1_2_9_44_1 e_1_2_9_7_1 e_1_2_9_5_1 e_1_2_9_3_1 e_1_2_9_9_1 e_1_2_9_25_1 e_1_2_9_27_1 e_1_2_9_48_1 e_1_2_9_29_1 |
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| Snippet | Candida albicans
is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is... Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is... is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal therapies is a medical need... Abstract Candida albicans is a frequent aetiologic agent of sepsis associated with high mortality in immunocompromised patients. Developing new antifungal... |
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| SubjectTerms | Animals Antifungal activity Antifungal agents Candida albicans Candida albicans - immunology Candida albicans - physiology Candidiasis Candidiasis - genetics Candidiasis - immunology Candidiasis - microbiology Clonal deletion Drug development Drug resistance EMBO19 EMBO23 EMBO28 Female Host-Pathogen Interactions - immunology Immune response Immunocompromised hosts Immunosuppressive agents infection Infections Inflammation Innate immunity Kidneys kinase inhibitor Leukocytes (neutrophilic) Macrophages Macrophages - immunology Macrophages - metabolism Macrophages - microbiology Mice, Inbred C57BL Mice, Knockout Mitogen-Activated Protein Kinase 12 - deficiency Mitogen-Activated Protein Kinase 12 - genetics Mitogen-Activated Protein Kinase 12 - immunology Mitogen-Activated Protein Kinase 13 - deficiency Mitogen-Activated Protein Kinase 13 - genetics Mitogen-Activated Protein Kinase 13 - immunology Mortality Mushrooms Myeloid cells Myeloid Cells - immunology Myeloid Cells - metabolism Myeloid Cells - microbiology Neutrophils - immunology Neutrophils - metabolism Neutrophils - microbiology Nitric Oxide Synthase Type II - immunology Nitric Oxide Synthase Type II - metabolism Nitric-oxide synthase p38MAPK Patients Reactive Oxygen Species - immunology Reactive Oxygen Species - metabolism Research Article Rodents Sepsis Septic shock Signal Transduction - genetics Signal Transduction - immunology signalling TAK1 protein Therapeutic applications |
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| Title | Myeloid cell deficiency of p38γ/p38δ protects against candidiasis and regulates antifungal immunity |
| URI | https://link.springer.com/article/10.15252/emmm.201708485 https://onlinelibrary.wiley.com/doi/abs/10.15252%2Femmm.201708485 https://www.ncbi.nlm.nih.gov/pubmed/29661910 https://www.proquest.com/docview/2035599651 https://www.proquest.com/docview/2026420979 https://pubmed.ncbi.nlm.nih.gov/PMC5938613 https://doaj.org/article/939e61b85a3b4a58b2f2dc2991a14ffb |
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