Common lung bacteria team up to evade immune defenses

The incidence of infection by Mycobacterium abscessus, is increasing in patients with cystic fibrosis, chronic obstructive pulmonary disease (COPD), and other chronic pulmonary diseases, leading to an accelerated lung function decline. Remarkably, 58–78% of patients with M. abscessus infection are also infected with Pseudomonas aeruginosa, the most common pathogen in these conditions. However, how these two bacterial species interact during infection remains poorly understood.

Now, a new study led by the Institute for Bioengineering of Catalonia (IBEC) and the Universitat Autònoma de Barcelona (UAB) has uncovered how co-infection by these two common lung pathogens can suppress immune responses and worsen outcomes in patients with respiratory diseases.

Using a combination of in vitro experiments on human bronchial cells and in vivo studies in insect models, the researchers demonstrated that when these two bacteria infect the body at the same time, the immune system becomes less effective at responding. The findings, published today in the journal Virulence, provide new insight into why polymicrobial infections are particularly difficult to treat and may lead to more severe disease.

"We found that M. abscessus and P. aeruginosa mutually inhibit the progression of single biofilms to form stable mixed biofilms".  Says Eduard Torrents, principal investigator of the Bacterial infections: antimicrobial therapies group at IBEC, Associate Professor at the University of Barcelona (UB), ICREA Academia member and author of the study. Biofilms are communities of bacteria that cluster together and secrete a protective matrix, which acts as a shield against antibiotics and the host immune system, making them a common cause of chronic infections.

"While each of these pathogens is dangerous on its own, their combined effect creates an environment in which the immune system is less able to respond". Adds Esther Julián, full professor of Microbiology at UAB, and author of the study. The results showed that the presence of both bacteria together led to a significant reduction in the production of key immune signalling molecules, effectively dampening the body's inflammatory response.

Coinfections may drive disease progression

Experiments conducted revealed that P. aeruginosa, when acting alone, triggers a strong immune response. This includes the overexpression of proinflammatory molecules and the activation of host defence mechanisms. However, when P. aeruginosa is present alongside M. abscessus, this immune response is significantly suppressed, suggesting an immunosuppressive effect driven by co-infection. These results were consistent across two bronchial epithelial cell lines and were also confirmed using Galleria mellonella larvae, a widely used animal model for studying infection. In these larvae, coinfections resulted in more rapid death compared to infections with either pathogen alone, reinforcing the conclusion that the immune system’s ability to fight infection is compromised in the presence of both bacteria​.

The study offers one of the first clear demonstrations of immune suppression caused by M. abscessus–P. aeruginosa coinfection and raises concerns about how such infections may contribute to therapy resistance and lung function decline, particularly in cystic fibrosis patients and other severe chronic lung disease​.

“Future treatments may need to go beyond antibiotics and include immune-modulating therapies to counteract the immune evasion strategies used by these bacteria.”, explains Víctor Campo-Pérez, first author of the study. Such approaches could help restore a more balanced immune response, improving the body’s ability to clear infections.

The findings highlight the complexity of polymicrobial infections and the importance of understanding how pathogens interact not just with the host, but also with each other, and open the door to new therapeutic strategies, particularly for vulnerable patients with chronic lung conditions.

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