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Researchers recently discovered that, in pulmonary diseases, M. abscessus suppresses immune responses during coinfection with P. aeruginosa.

Mycobacterium abscessus significantly suppresses host immune responses during coinfection with Pseudomonas aeruginosa, exacerbating pulmonary disease outcomes, according to findings published in Virulence.

“The incidence of infection by nontuberculous mycobacteria, mainly Mycobacterium abscessus, is increasing in patients with cystic fibrosis and other chronic pulmonary diseases, leading to an accelerated lung function decline. In most cases, M. abscessus coinfects Pseudomonas aeruginosa, the most common pathogen in these conditions,” wrote Eduard Torrents, PhD, of University of Barcelona and colleagues. “However, how these two bacterial species interact during infection remains poorly understood.”

Enhancing Understanding

To enhance understanding of this interaction, the research team integrated in vitro coculture experiments in two bronchial epithelial cell lines with in vivo validation in Galleria mellonella larvae. They compared single-species infections of laboratory (P. aeruginosa PAO1) and clinical (P. aeruginosa PAET1) strains, as well as rough and smooth morphotypes of M. abscessus, against mixed infections, assessing biofilm dynamics, epithelial viability, cytokine profiles, and host-survival endpoints.

According to the study, key findings included:

• Mutual biofilm restraint: Introduction of live abscessus—regardless of morphotype—reduced expansion of pre-formed or developing P. aeruginosa biofilms, while P. aeruginosa similarly restricted mycobacterial biofilms, suggesting intense nutrient competition and possible quorum-signal interference.
• Blunted epithelial signaling: Whereas aeruginosa alone provoked robust IL-6/IL-8 release via toll-like receptor (TLR)2/TLR5 pathways, mixed infection suppressed this response to levels seen with M. abscessus alone, implying an immunomodulatory effect of glycopeptidolipids or other TLR antagonists. Cell viability loss was greatest under coinfection, despite attenuated cytokine output.
• Accelerated lethality in vivo: In larvae, coinfection shortened survival relative to either pathogen alone and sharply down-regulated antimicrobial peptides, transferrin, and pro-phenoloxidase genes, demonstrating systemic immune paralysis.

The authors noted that although the laboratory strains behaved comparably to the clinical isolate, they recommend testing additional clinical strains to confirm generalizability.

“Immune Quiet” Niche

For pulmonologists managing advanced CF or COPD, the data suggest that dual colonization may create an “immune quiet” niche that shields both organisms from host clearance and standard antibiotic regimens, even though each restrains the other’s biofilm growth, according to the authors. They suggested that immunologic biomarkers could therefore underestimate pathogen load, and anti-inflammatory therapy may need re-evaluation when both bacteria are present.

“Overall, this study highlights the novel role of M. abscessus in suppressing immune responses during coinfection with P. aeruginosa, emphasizing the clinical implications for the management of cystic fibrosis and other pulmonary diseases,” the researchers concluded. “Understanding these interactions could inform the development of new therapeutic strategies to mitigate the severity of coinfections in vulnerable patients.”