Mycobacterium avium complex infected cells promote growth of the pathogen Pseudomonas aeruginosa

Bronchiectasis is considered a consequence of the neutrophilic inflammatory response to infection. Mycobacterial infections, mainly from the Mycobacterium avium complex and M. abscessus, have been inextricably linked to bronchiectasis development. The most important pathogen that infect patients wit...

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Published in:Microbial pathogenesis Vol. 166; p. 105549
Main Authors: Carazo-Fernández, Luis, González-Cortés, Carolina, López-Medrano, Ramiro, Diez-Tascón, Cristina, Marcos-Benavides, María Francisca, Rivero-Lezcano, Octavio Miguel
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01-05-2022
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Summary:Bronchiectasis is considered a consequence of the neutrophilic inflammatory response to infection. Mycobacterial infections, mainly from the Mycobacterium avium complex and M. abscessus, have been inextricably linked to bronchiectasis development. The most important pathogen that infect patients with bronchiectasis is Pseudomonas aeruginosa, associated with an increased risk of death. Patients with bronchiectasis are often co-infected with P. aeruginosa and M. avium complex, and it was studied whether they interacted in immune cell cultures. Peripheral blood mononuclear cells from healthy volunteers were infected overnight with clinical isolates of mycobacteria, 18 h later co-infected with P. aeruginosa and Pseudomonas multiplication was quantified. Inoculated P. aeruginosa multiply faster when cells were previously infected in vitro with M. avium complex or M. tuberculosis, but not with M. kansasii or M. gordonae, mycobacteria not regularly isolated from patients with bronchiectasis. The interaction between mycobacteria and P. aeruginosa also takes place in the absence of cells, but to a lower degree. Growth of Staphylococcus aureus, less frequently co-isolated with mycobacteria, was not affected by previous infection with mycobacteria. Surprisingly, multiplication of P. aeruginosa in neutrophil cultures did not vary in the presence of mycobacteria. Nevertheless, co-infection of mycobacteria and P. aeruginosa induced the production of IL-1β, a mediator of neutrophilic inflammation. P. aeruginosa stimulation by mycobacteria provides evidence for explaining their common clinical association. Strategies to control mycobacteria may be useful to impair P. aeruginosa colonization. •M. avium complex and M. tuberculosis co-infected cells promote P. aeruginosa growth.•Peripheral blood mononuclear cells, but not neutrophils, promote growth.•Less pathogenic mycobacteria (e.g. M. gordonae) do not promote growth.•Co-infected cells produce IL-1β, mediator of neutrophilic inflammation.•Observed mycobacteria - P. aeruginosa interaction may have clinical relevance.
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ISSN:0882-4010
1096-1208
DOI:10.1016/j.micpath.2022.105549