Eosinophils are part of the granulocyte response in tuberculosis and promote host resistance in mice-Reference-Cited by-同舟云学术

Eosinophils are part of the granulocyte response in tuberculosis and promote host resistance in mice

Published:2021-08-04 Issue:10 Volume:218 Page:
ISSN:0022-1007
Container-title:Journal of Experimental Medicine
language:en
Short-container-title:

Author:

Bohrer Andrea C.¹^ORCID,Castro Ehydel¹^ORCID,Hu Zhidong²³^ORCID,Queiroz Artur T.L.⁴^ORCID,Tocheny Claire E.¹^ORCID,Assmann Maike¹^ORCID,Sakai Shunsuke⁵^ORCID,Nelson Christine⁵^ORCID,Baker Paul J.¹^ORCID,Ma Hui²³^ORCID,Wang Lin³⁶^ORCID,Zilu Wen³⁶^ORCID,du Bruyn Elsa⁷^ORCID,Riou Catherine⁷^ORCID,Kauffman Keith D.⁵^ORCID,Moore Ian N.⁸^ORCID,Del Nonno Franca⁹^ORCID,Petrone Linda¹⁰^ORCID,Goletti Delia¹⁰^ORCID,Martineau Adrian R.¹¹^ORCID,Lowe David M.¹¹^ORCID,Cronan Mark R.¹²¹³^ORCID,Wilkinson Robert J.⁷¹⁴¹⁵^ORCID,Barry Clifton E.⁷¹⁶^ORCID,Via Laura E.¹⁷¹⁶^ORCID,Barber Daniel L.⁵^ORCID,Klion Amy D.¹⁸^ORCID,Andrade Bruno B.⁴^ORCID,Song Yanzheng³⁶^ORCID,Wong Ka-Wing²³^ORCID,Mayer-Barber Katrin D.¹^ORCID,

Affiliation:

1. Inflammation and Innate Immunity Unit, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

2. Department of Scientific Research, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China

3. Tuberculosis Center, Shanghai Emerging and Re-emerging Infectious Disease Institute, Fudan University, Shanghai, China

4. The KAB group, Multinational Organization Network Sponsoring Translational and Epidemiological Research Initiative, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador Brazil

5. T Lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

6. Department of Thoracic Surgery, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China

7. Wellcome Centre for Infectious Diseases Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, South Africa

8. Infectious Disease Pathogenesis Section, Comparative Medicine Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

9. Pathology Unit, National Institute for Infectious Diseases “L. Spallanzani,” Istituto Di Ricovero e Cura a Carattere Scientifico, Rome, Italy

10. Translational Research Unit, Department of Epidemiology and Preclinical Research National Institute for Infectious Diseases, Istituto Di Ricovero e Cura a Carattere Scientifico, Rome, Italy

11. Institute of Immunity and Transplantation, University College London, London, UK

12. In Vivo Cell Biology of Infection Unit, Max Planck Institute for Infection Biology, Berlin, Germany

13. Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC

14. Department of Infectious Diseases, Imperial College London, UK

15. Francis Crick Institute, London, UK

16. Tuberculosis Research Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

17. Tuberculosis Imaging Program, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

18. Human Eosinophil Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

Abstract

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.

Funder

Division of Intramural Research, National Institute of Allergy and Infectious Diseases

National Natural Science Foundation of China

National Institutes of Health

Wellcome Trust

Cancer Research UK

UK Research and Innovation

National Council for Scientific and Technological Development

Oswaldo Cruz Foundation

Publisher

Rockefeller University Press

Subject