Alpha1-antitrypsin impacts innate host-pathogen interactions with

Filamentous growth Immune escape cell wall remodelling fungal adaptation host-pathogen interactions immune evasion

Journal

Virulence
ISSN: 2150-5608
Titre abrégé: Virulence
Pays: United States
ID NLM: 101531386

Informations de publication

Date de publication:
22 Mar 2024
Historique:
medline: 22 3 2024
pubmed: 22 3 2024
entrez: 22 3 2024
Statut: aheadofprint

Résumé

Our immune system possesses sophisticatedmechanisms to cope with invading microorganisms, while pathogensevolve strategies to deal with threats imposed by host immunity. Thehuman plasma protein α1-antitrypsin (AAT) exhibits pleiotropicimmune-modulating properties by both preventing immunopathology andimproving antimicrobial host defence. Genetic associations suggesteda role for AAT in candidemia, the most frequent fungal bloodstreaminfection in the ICU, yet little is known about how AAT influencesinteractions between

Identifiants

DOI: 10.1080/21505594.2024.2333367 PMID: 38515333
pubmed: 38515333
doi: 10.1080/21505594.2024.2333367
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2333367

Auteurs

Martin Jaeger (M)

Department of Medicine, University of Colorado Denver, Aurora.
Department of Internal Medicine, Radboud University Medical Center and Radboud Center for Infectious diseases (RCI).
Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University Nijmegen Medical Center (Radboudumc), Nijmegen, The Netherlands.

Axel Dietschmann (A)

Junior Research Group Adaptive Pathogenicity Strategies, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute, Jena, Germany.

Sophie Austermeier (S)

Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute, Jena, Germany.

Sude Dinçer (S)

Junior Research Group Adaptive Pathogenicity Strategies, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute, Jena, Germany.

Pauline Porschitz (P)

Junior Research Group Adaptive Pathogenicity Strategies, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute, Jena, Germany.

Larsen Vornholz (L)

Institute of Clinical Chemistry and Pathobiochemistry, School of Medicine, Technical University of Munich, Munich, Germany.

Ralph J A Maas (RJA)

Department of Medicine, University of Colorado Denver, Aurora.
Department of Laboratory Medicine, Laboratory of Hematology, Radboud University Medical Center, Nijmegen, The Netherlands.

Evelien G G Sprenkeler (EGG)

Department of Internal Medicine, Radboud University Medical Center and Radboud Center for Infectious diseases (RCI).

Jürgen Ruland (J)

Institute of Clinical Chemistry and Pathobiochemistry, School of Medicine, Technical University of Munich, Munich, Germany.

Stefan Wirtz (S)

Medizinische Klinik 1, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.

Tania Azam (T)

Department of Medicine, University of Colorado Denver, Aurora.

Leo A B Joosten (LAB)

Department of Internal Medicine, Radboud University Medical Center and Radboud Center for Infectious diseases (RCI).

Bernhard Hube (B)

Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute, Jena, Germany.
Institute of Microbiology, Friedrich-Schiller-University, Jena, Germany.

Mihai G Netea (MG)

Department of Internal Medicine, Radboud University Medical Center and Radboud Center for Infectious diseases (RCI).

Charles A Dinarello (CA)

Department of Medicine, University of Colorado Denver, Aurora.
Department of Internal Medicine, Radboud University Medical Center and Radboud Center for Infectious diseases (RCI).

Mark S Gresnigt (MS)

Department of Medicine, University of Colorado Denver, Aurora.
ORCID: 0000-0002-9514-4634

Classifications MeSH