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

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....

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Published inThe Journal of experimental medicine Vol. 218; no. 10
Main Authors Bohrer, Andrea C, Castro, Ehydel, Hu, Zhidong, Queiroz, Artur T L, Tocheny, Claire E, Assmann, Maike, Sakai, Shunsuke, Nelson, Christine, Baker, Paul J, Ma, Hui, Wang, Lin, Zilu, Wen, du Bruyn, Elsa, Riou, Catherine, Kauffman, Keith D, Moore, Ian N, Del Nonno, Franca, Petrone, Linda, Goletti, Delia, Martineau, Adrian R, Lowe, David M, Cronan, Mark R, Wilkinson, Robert J, Barry, Clifton E, Via, Laura E, Barber, Daniel L, Klion, Amy D, Andrade, Bruno B, Song, Yanzheng, Wong, Ka-Wing, Mayer-Barber, Katrin D
Format Journal Article
LanguageEnglish
Published United States Rockefeller University Press 04.10.2021
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Summary: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.
Bibliography: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.
A.C. Bohrer, E. Castro, and Z. Hu contributed equally to this paper.
ISSN:0022-1007
1540-9538
DOI:10.1084/jem.20210469