Researchers from Netherlands Finds That COVID-19 Antibodies Can Trigger Dangerous Inflammation
Nikhil Prasad Fact checked by:Thailand Medical News Team Dec 21, 2025 1 hour, 36 minutes ago
Medical News: Antibodies That Help May Also Harm
Scientists are continuing to uncover why some people develop severe COVID-19 while others recover quickly. A new study has revealed a troubling twist. Certain antibodies meant to protect the body may actually fuel dangerous inflammation in the lungs. This
Medical News report highlights how specific COVID-19 antibodies can overstimulate immune cells and worsen disease outcomes instead of preventing them.
Certain COVID-19 antibodies may overstimulate immune cells and fuel severe inflammation rather than
protect the lungs
The Role of Macrophages in Severe COVID
Macrophages are frontline immune cells found in the lungs. Their job is to destroy invading pathogens and coordinate immune responses. However, researchers found that in severe COVID-19 cases, these cells can become overactivated. The trigger is not just the virus itself but immune complexes formed when anti-spike IgG antibodies bind to the SARS-CoV-2 spike protein.
How Antibodies Rewire Immune Cell Metabolism
The study showed that when human macrophages encounter these antibody-virus complexes, their internal metabolism rapidly changes. The cells begin consuming more glucose and activating fatty acid production pathways. This metabolic rewiring provides excess energy and building materials that drive the release of powerful inflammatory chemicals such as interleukin-6. These substances contribute to lung swelling, blood clot formation, and tissue damage.
Virus Alone Is Not the Main Driver
Surprisingly, viral signals alone did not cause this intense inflammatory response. The excessive inflammation only occurred when viral signals were combined with anti-spike IgG antibodies. Even more concerning, the metabolic changes inside macrophages were triggered mainly by the antibodies themselves, showing that the immune response after antibody formation can be a critical danger phase.
Blocking Metabolism Reduces Inflammation
Researchers tested several metabolic blockers to see if inflammation could be controlled. When glucose breakdown, fatty acid synthesis, or the pentose phosphate pathway were inhibited, inflammatory cytokine production dropped sharply. This suggests that targeting immune cell metabolism may be an effective strategy to reduce severe COVID-19 complications without suppressing the entire immune system.
Mitochondrial Stress Adds to the Damage
The study also found signs of early mitochondrial stress in macrophages exposed to anti-spike antibodies. Mitochondria are the power plants of cells, and their dysfunction can further amplify inflammation. These findings help explain why inflammation can escalate rapidly in critically ill patients.
Who Conducted the Study
The research was carried out by scientists from Amsterdam University Medical Center, Leiden University Medical Center, Vrije Universiteit Amsterdam, and multip
le affiliated institutes within the Netherlands, including the Amsterdam Institute for Immunology and Infectious Diseases and the Amsterdam Cardiovascular Sciences Institute.
Why These Findings Matter
The conclusions suggest that severe COVID-19 is not just a viral disease but also an antibody-driven inflammatory disorder. Understanding how antibodies alter immune metabolism opens the door to new treatments that calm harmful inflammation while preserving protective immunity. This approach could improve outcomes for high-risk patients and guide future therapeutic strategies.
The study findings were published in the peer reviewed journal: European Journal of Immunology
https://onlinelibrary.wiley.com/doi/10.1002/eji.70087
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https://www.thailandmedical.news/articles/coronavirus
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