Each year, hundreds of thousands of people in Germany experience a stroke or heart attack, conditions that are not only life-threatening on their own but also make patients more susceptible to dangerous bacterial infections due to immune disturbances.
Researchers from the University Hospital of the University of Duisburg-Essen and the Leibniz Institute for Analytical Sciences have made a significant breakthrough in understanding and potentially treating this vulnerability.
Published in Nature Cardiovascular Research, the study led by Prof. Matthias Gunzer and Dr. Vikramjeet Singh identifies a dramatic reduction in IgA antibodies—crucial defenders against infections—as a key factor in the immune dysfunction following a stroke or heart attack.
Immunoglobulins like IgA are produced by plasma cells and are vital in combating pathogens.
The research teams discovered that this reduction in antibodies is linked to neutrophil extracellular traps (NETs), which are networks of DNA fibers released from neutrophils, a type of white blood cell.
After a stroke or heart attack, these NETs are released in large quantities and have a dual detrimental effect. They directly destroy plasma cells in the intestines and create numerous small clots in blood vessels.
These clots block the supply of nutrients and oxygen to the plasma cells, leading to their death and a consequent plunge in antibody levels.
The study’s insights were garnered through disease mouse models, which mirrored the human condition of post-stroke and heart attack immune compromise.
The researchers found that by breaking down these NETs with an enzyme called DNase, or by preventing their formation using a new substance, they could preserve the immune system’s function. These interventions proved effective in both animal models and subsequent clinical studies.
Prof. Gunzer highlights the significance of these findings, stating that the ability to either dismantle NETs or prevent their formation could lead to revolutionary treatments.
These treatments could maintain immune defense in patients after cardiovascular events, potentially preventing severe secondary infections or even death.
This discovery opens a promising new avenue for clinical interventions that could greatly improve outcomes for stroke and heart attack survivors, addressing a previously unmet medical need by tackling the underlying causes of post-event immune deficiencies.
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The research findings can be found in Nature Cardiovascular Research.
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