Anakinra reduces lung inflammation in experimental acute lung injury.
IL-1
IL-1Ra
covid-19
immunotherapy
respiratory distress syndrome
Journal
Immunity, inflammation and disease
ISSN: 2050-4527
Titre abrégé: Immun Inflamm Dis
Pays: England
ID NLM: 101635460
Informations de publication
Date de publication:
02 2022
02 2022
Historique:
revised:
17
09
2021
received:
25
06
2021
accepted:
05
10
2021
pubmed:
11
12
2021
medline:
22
1
2022
entrez:
10
12
2021
Statut:
ppublish
Résumé
Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury (ALI) resulting in life-threatening hypoxaemia. Although ARDS can be caused by a variety of pathogens or major trauma, it is best known as the major cause of mortality in COVID-19 patients. Since ARDS is often associated with dysregulated inflammatory immune responses, immunomodulatory approaches represent a possible treatment option. The objective of this study was to evaluate the therapeutic potential of interleukin (IL)-1 blockade using Anakinra in a mouse model of lipopolysaccharide (LPS)-induced ALI. We evaluated the effects of a daily subcutaneous Anakinra treatment in a mouse model of LPS-induced ALI. We monitored body weight to assess the general health status of the mice. Two days after ALI induction, we evaluated the inflammatory cytokine MIP-2 as well as protein levels in bronchoalveolar lavage (BAL) fluids. Two and nine days after ALI induction, we evaluated infiltrating leukocytes in BAL fluid and lung tissue. Anakinra treatment reduced ALI-induced weight loss compared to nontreated groups. At Day 2, Anakinra treatment reduced levels of MIP-2 and protein in BAL fluids and reduced frequencies of NK cells and neutrophils in the lung tissue. Nine days after ALI induction, Anakinra treated mice displayed reduced levels of neutrophils and alveolar macrophages in BAL fluids. IL-1 blockade using Anakinra reduced classical hallmarks of inflammation in a mouse model of ALI. Our data support ongoing and future research on the evaluation of Anakinra as a potential treatment option in ARDS.
Identifiants
pubmed: 34889061
doi: 10.1002/iid3.548
pmc: PMC8767508
doi:
Substances chimiques
Interleukin 1 Receptor Antagonist Protein
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
123-129Subventions
Organisme : Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
ID : P2BEP3_188262
Organisme : Agence Nationale de la Recherche
ID : ANR-11-IDEX-0004-02
Organisme : Agence Nationale de la Recherche
ID : LabEx Transimmunom
Informations de copyright
© 2021 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.
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