Eosinophils are part of the granulocyte response in tuberculosis and promote host resistance in mice.
Adult
Animals
Eosinophils
/ physiology
Female
Granulocytes
/ microbiology
Host-Pathogen Interactions
/ physiology
Humans
Latent Tuberculosis
/ microbiology
Lung
/ microbiology
Macaca mulatta
Male
Mice, Mutant Strains
Mycobacterium tuberculosis
/ pathogenicity
Tuberculosis
/ drug therapy
Zebrafish
/ microbiology
Journal
The Journal of experimental medicine
ISSN: 1540-9538
Titre abrégé: J Exp Med
Pays: United States
ID NLM: 2985109R
Informations de publication
Date de publication:
04 10 2021
04 10 2021
Historique:
received:
24
02
2021
revised:
16
05
2021
accepted:
13
07
2021
entrez:
4
8
2021
pubmed:
5
8
2021
medline:
15
12
2021
Statut:
ppublish
Résumé
Host resistance to Mycobacterium tuberculosis (Mtb) infection requires the activities of multiple leukocyte subsets, yet the roles of the different innate effector cells during tuberculosis are incompletely understood. Here we uncover an unexpected association between eosinophils and Mtb infection. In humans, eosinophils are decreased in the blood but enriched in resected human tuberculosis lung lesions and autopsy granulomas. An influx of eosinophils is also evident in infected zebrafish, mice, and nonhuman primate granulomas, where they are functionally activated and degranulate. Importantly, using complementary genetic models of eosinophil deficiency, we demonstrate that in mice, eosinophils are required for optimal pulmonary bacterial control and host survival after Mtb infection. Collectively, our findings uncover an unexpected recruitment of eosinophils to the infected lung tissue and a protective role for these cells in the control of Mtb infection in mice.
Identifiants
pubmed: 34347010
pii: 212535
doi: 10.1084/jem.20210469
pmc: PMC8348215
pii:
doi:
Types de publication
Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Wellcome Trust
ID : FC0010218
Pays : United Kingdom
Organisme : NIH HHS
ID : U01AI115940
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI115940
Pays : United States
Organisme : Intramural NIH HHS
Pays : United States
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 203135
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 104803
Pays : United Kingdom
Organisme : Cancer Research UK
Pays : United Kingdom
Informations de copyright
© 2021 Bohrer et al.
Déclaration de conflit d'intérêts
Disclosures: D.M. Lowe reported personal fees from Merck, non-financial support from CSL Behring, and non-financial support from Fujifilm Chemical Co. outside the submitted work. No other disclosures were reported.
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