Host lung microbiota promotes malaria-associated acute respiratory distress syndrome

Debanjan Mukherjee, Ângelo Ferreira Chora, Jean-Christophe Lone, Ricardo S. Ramiro, Birte Blankenhaus, Karine Serre, Mário Ramirez, Isabel Gordo, Marc Veldhoen, Patrick Varga-Weisz and Maria M. Mota ()
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Debanjan Mukherjee: Faculdade de Medicina da Universidade de Lisboa
Ângelo Ferreira Chora: Faculdade de Medicina da Universidade de Lisboa
Jean-Christophe Lone: Faculdade de Medicina da Universidade de Lisboa
Ricardo S. Ramiro: Instituto Gulbenkian de Ciência
Birte Blankenhaus: Faculdade de Medicina da Universidade de Lisboa
Karine Serre: Faculdade de Medicina da Universidade de Lisboa
Mário Ramirez: Faculdade de Medicina da Universidade de Lisboa
Isabel Gordo: Instituto Gulbenkian de Ciência
Marc Veldhoen: Faculdade de Medicina da Universidade de Lisboa
Patrick Varga-Weisz: University of Essex
Maria M. Mota: Faculdade de Medicina da Universidade de Lisboa

Nature Communications, 2022, vol. 13, issue 1, 1-14

Abstract: Abstract Severe malaria can manifest itself with a variety of well-recognized clinical phenotypes that are highly predictive of death – severe anaemia, coma (cerebral malaria), multiple organ failure, and respiratory distress. The reasons why an infected individual develops one pathology rather than another remain poorly understood. Here we use distinct rodent models of infection to show that the host microbiota is a contributing factor for the development of respiratory distress syndrome and host mortality in the context of malaria infections (malaria-associated acute respiratory distress syndrome, MA-ARDS). We show that parasite sequestration in the lung results in sustained immune activation. Subsequent production of the anti-inflammatory cytokine IL-10 by T cells compromises microbial control, leading to severe lung disease. Notably, bacterial clearance with linezolid, an antibiotic commonly used in the clinical setting to control lung-associated bacterial infections, prevents MA-ARDS-associated lethality. Thus, we propose that the host’s anti-inflammatory response to limit tissue damage can result in loss of microbial control, which promotes MA-ARDS. This must be considered when intervening against life-threatening respiratory complications.

Date: 2022
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-31301-8

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DOI: 10.1038/s41467-022-31301-8

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