Alveolar macrophage metabolic programming via a C-type lectin receptor protects against lipo-toxicity and cell death

Michal Scur, Ahmad Bakur Mahmoud, Sayanti Dey, Farah Abdalbarri, Iona Stylianides, Daniel Medina-Luna, Gayani S. Gamage, Aaron Woblistin, Alexa N. M. Wilson, Haggag S. Zein, Ashley Stueck, Andrew Wight, Oscar A. Aguilar, Francesca Di Cara, Brendon D. Parsons, Mir Munir A. Rahim, James R. Carlyle and Andrew P. Makrigiannis ()
Additional contact information
Michal Scur: Dalhousie University
Ahmad Bakur Mahmoud: Taibah University
Sayanti Dey: Dalhousie University
Farah Abdalbarri: McGill University
Iona Stylianides: Dalhousie University
Daniel Medina-Luna: Dalhousie University
Gayani S. Gamage: Dalhousie University
Aaron Woblistin: Dalhousie University
Alexa N. M. Wilson: Dalhousie University
Haggag S. Zein: Dalhousie University
Ashley Stueck: Dalhousie University
Andrew Wight: Dana-Farber Cancer Institute
Oscar A. Aguilar: University of California
Francesca Di Cara: Dalhousie University
Brendon D. Parsons: Dalhousie University
Mir Munir A. Rahim: University of Windsor
James R. Carlyle: University of Toronto
Andrew P. Makrigiannis: Dalhousie University

Nature Communications, 2022, vol. 13, issue 1, 1-20

Abstract: Abstract Alveolar macrophages (AM) hold lung homeostasis intact. In addition to the defense against inhaled pathogens and deleterious inflammation, AM also maintain pulmonary surfactant homeostasis, a vital lung function that prevents pulmonary alveolar proteinosis. Signals transmitted between AM and pneumocytes of the pulmonary niche coordinate these specialized functions. However, the mechanisms that guide the metabolic homeostasis of AM remain largely elusive. We show that the NK cell-associated receptor, NKR-P1B, is expressed by AM and is essential for metabolic programming. Nkrp1b−/− mice are vulnerable to pneumococcal infection due to an age-dependent collapse in the number of AM and the formation of lipid-laden AM. The AM of Nkrp1b−/− mice show increased uptake but defective metabolism of surfactant lipids. We identify a physical relay between AM and alveolar type-II pneumocytes that is dependent on pneumocyte Clr-g expression. These findings implicate the NKR-P1B:Clr-g signaling axis in AM-pneumocyte communication as being important for maintaining metabolism in AM.

Date: 2022
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DOI: 10.1038/s41467-022-34935-w

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