A new study published in Virulence reveals how lung infections involving more than one type of bacteria suppress the immune system.
Mycobacterium abscessus and Pseudomonas aeruginosa often coinfect patients with chronic lung conditions. People with cystic fibrosis (CF) or chronic obstructive pulmonary disease (COPD) are especially at risk.
Why Do Lung Coinfections Lead to Worse Health Outcomes?
The study explains why these coinfections lead to worse health outcomes. Coinfecting bacteria form stable, mixed biofilms that resist treatment.
Biofilms are dense clusters of bacteria surrounded by a protective barrier. This matrix shields bacteria from antibiotics and immune system attacks. Mixed biofilms are harder to treat than infections with one bacterium.
Each bacterium triggers strong immune activity when acting alone. But together, they suppress immune signals and reduce inflammation. This helps the bacteria survive longer and worsen the disease. The study offers new insight into how these pathogens interact.
How did Researchers Show that Bacterial Coinfections Are Harder to Treat?
Researchers tested how coinfections affect bacterial growth and immune response. They used two P. aeruginosa strains: PAO1 and PAET1. PAO1 is a standard reference strain with antibiotic resistance. PAET1 is a clinical strain from a chronic cystic fibrosis case.
Mature P. aeruginosa biofilms were grown for 72 hours. Researchers then exposed them to other bacteria for 24 hours. They measured changes in light intensity to track biofilm growth. Each result was compared to P. aeruginosa grown in isolation.
Mycobacterium abscessus biofilms were grown separately for five days. Then P. aeruginosa was added and grown for three more days. These dual-species biofilms were also compared to single-species controls. Together, the bacteria reduced each other’s biofilm growth but survived.
To test immune effects, researchers used moth (Galleria mellonella) larvae. Each larva received 10 microliters of bacterial suspension. Thirty larvae were exposed to various bacteria combinations.
Researchers also infected two types of human lung cells. They tested single infections and coinfections for comparison. M. abscessus or B. thuringiensis alone caused only mild damage. But coinfections with P. aeruginosa caused much more cell death.
The most damaging combination was P. aeruginosa with M. abscessus R. Across all models, co-infection suppressed immune responses significantly. The bacteria together triggered less inflammation than either alone. These findings help explain why coinfections are harder to treat.
What Implications did Researchers Identify Based on these Findings?
Researchers identified P. aeruginosa as the most dangerous coinfecting pathogen. It forms biofilms that resist both antibiotics and immune system defenses. Other bacteria, including S. aureus and M. abscessus, also play harmful roles. M. abscessus is growing in importance due to drug resistance and biofilms.
P. aeruginosa was the more dominant strain in these experiments. This is likely due to its much faster replication rate. No toxic compounds caused inhibition between the two strains. Instead, competition for space and nutrients limited bacterial growth.
Coinfection may increase antibiotic resistance over time. If P. aeruginosa is killed off, M. abscessus may expand. This reflects its ability to persist and spread even in competition. Such dynamics should be considered in cystic fibrosis treatment plans.
Dual infection may lead to chronic disease and faster lung decline. Future research must continue exploring these bacterial interactions. New treatments should target both bacterial growth and immune imbalance. Possible approaches include biofilm disruptors, phage therapy, and immune modulators.
More clinical strains should be tested to confirm these results. A broader strain range could reveal consistent patterns in coinfection. This knowledge may help improve treatment for chronic lung disease patients.
Conclusion
Co-infection with M. abscessus and P. aeruginosa suppresses immune responses and worsens outcomes. These bacteria form stable mixed biofilms and damage lung cells more severely. New treatments must address both bacterial survival and immune system disruption.
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Logan Hamilton is a health and wellness freelance writer for hire. He’s passionate about crafting crystal-clear, captivating, and credible content that elevates brands and establishes trust. When not writing, Logan can be found hiking, sticking his nose in bizarre books, or playing drums in a local rock band. Find him at loganjameshamilton.com.
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