P001

1:Institut de Bioenginyeria de Catalunya (IBEC); 2:Universitat de Barcelona; 3:Universitat Autònoma de Barcelona

The incidence of infection caused by nontuberculous mycobacteria, mainly Mycobacterium abscessus, is increasing in patients with cystic fibrosis and other chronic pulmonary illnesses, translating into an accelerated decline in lung function. In most cases, M. abscessus co-infects Pseudomonas aeruginosa, the most common pathogen in these chronic diseases. However, the interactions between these two bacterial species during infection remain largely unknown.

This study aimed to explore the behaviour of both species in three relevant pathogenic settings. We employed a dual-species biofilm development approach using a recently developed method to monitor individual species within dual-species biofilms. Additionally, we conducted co-infection studies in bronchial epithelial cells using in vitro assays and in vivo co-infection studies using the Galleria mellonella model.

The results revealed that both species can form stable mixed biofilms while reciprocally inhibiting single-species biofilm progression. Co-infections in bronchial epithelial cells were associated with significantly reduced cell viability. Similarly, in G. mellonella, co-infections resulted in lower survival rates compared to infections by either species alone. Analysis of the immune response triggered by each bacterium in bronchial epithelial cells and G. mellonella larvae demonstrated that P. aeruginosa induces the overexpression of the proinflammatory response and activation of the melanization cascade. In contrast, co-infection with M. abscessus and P. aeruginosa significantly suppressed immune responses in both models, leading to more severe outcomes for the host compared to single-species infections by P. aeruginosa.

Overall, the presence of M. abscessus compromises the host’s immune response, exacerbating infection and resulting in worse outcomes for the host.