Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 01, 2026 1 hour, 5 minutes ago
Scientists identify a hidden chain reaction that blocks blood flow in the lungs and worsens COVID-19
A new study has uncovered an important mechanism behind the dangerous lung complications seen in severe COVID-19. Researchers have discovered that neutrophils, a type of white blood cell that normally helps fight infections, can become unusually sticky after SARS-CoV-2 infection. Instead of moving freely through the bloodstream, these immune cells attach themselves to the walls of tiny lung blood vessels, creating the perfect environment for blood clots to develop.
Scientists discover that sticky neutrophils trap platelets inside lung blood vessels, driving the formation of dangerous
microclots in COVID-19.
The research was conducted by scientists from The University of Tokyo, Academia Sinica in Taipei, Taiwan, Chiba University, Japan's National Institute of Infectious Diseases, and Gunma University Graduate School of Medicine. Their findings provide new insight into how severe COVID-19 damages the lungs and point to a promising target for future treatments.
Scientists Captured the Process as It Happened
To understand exactly how these harmful clots form, the research team used advanced two-photon excitation microscopy in a Biosafety Level 3 laboratory. This cutting-edge imaging technology enabled them to observe the lungs of obese mice infected with a fluorescent SARS-CoV-2 virus in real time.
The researchers tracked neutrophil movement inside tiny lung blood vessels, measured platelet aggregation, monitored blood flow through lung capillaries, and examined changes in adhesion molecules expressed by neutrophils. They also re-analyzed single-cell RNA sequencing data from patients with severe COVID-19 to determine whether the same biological changes occurred in humans.
Sticky Neutrophils Become the Foundation for Blood Clots
The study revealed that SARS-CoV-2 infection dramatically increased the amount of time neutrophils remained attached to pulmonary blood vessel walls. This prolonged adhesion was driven by increased expression of the adhesion molecules CD44, CD62L, and E-selectin, making the immune cells far stickier than under normal conditions.
Once immobilized, these neutrophils acted like biological anchors that trapped passing platelets. As additional platelets accumulated, the growing platelet-neutrophil complexes gradually developed into microthrombi—tiny blood clots capable of obstructing the smallest blood vessels in the lungs. The resulting blockages significantly impaired pulmonary circulation, reducing the efficient delivery of oxygen into the bloodstream.
In this
Medical News report, the findings suggest that microclot formation in severe COVID-19 follows a well-defined sequence rather than occurring randomly. The disease appears to begin with abnormal neutrophil adhesion, followed by platelet capture and progressive clot formation that eventually disrupts lung perfusion.
Reducing Neutrophils Improved Survival
The investigators also t
ested what would happen if neutrophils were removed. They found that neutrophil depletion significantly reduced microthrombus formation, improved blood flow through the lungs, and extended survival in infected mice. These results strongly suggest that neutrophils play a central role in driving the clotting process rather than merely responding to it.
Importantly, analysis of human single-cell RNA sequencing datasets showed that neutrophils from patients with severe COVID-19 expressed markedly higher levels of CD44 and SELL, the gene encoding CD62L. This close agreement between laboratory findings and patient data strengthens the evidence that the same mechanism contributes to severe disease in humans.
A Promising New Target for COVID-19 Treatment
The discovery raises the possibility that future therapies could focus on preventing neutrophils from adhering to blood vessel walls before dangerous clots begin to develop. Targeting the adhesion molecules responsible for this process may help preserve lung blood flow, reduce tissue damage, and improve outcomes for patients with severe COVID-19.
Conclusion
The study provides compelling evidence that sticky neutrophils are a crucial trigger for the formation of lung microclots in severe COVID-19. By uncovering the molecular events that transform these immune cells into platforms for platelet accumulation, the researchers have identified a potential therapeutic strategy that could interrupt clot formation at its earliest stage, preserve pulmonary circulation, and ultimately improve survival in patients facing severe SARS-CoV-2 infection.
The study findings were published in the peer reviewed journal: The Journal of Immunology.
https://academic.oup.com/jimmunol/article/215/Supplement_1/vkag141.1545/8745769
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