Strange Immune Cell Shifts Seen in COVID-19 Patients Hint at Early Bone Marrow Reprogramming!
Nikhil Prasad Fact checked by:Thailand Medical News Team May 16, 2025 8 hours, 38 minutes ago
Medical News: A team of scientists from multiple institutions in France and the United States has uncovered how certain innate immune cells in the blood behave abnormally during the early stages of COVID-19, possibly due to deep changes in how these cells are formed in the bone marrow. The study, which involved hospitalized COVID-19 patients in Lille, France, tracked immune cell changes over a 30-day period to better understand the body’s response to SARS-CoV-2 infection.
Strange Immune Cell Shifts Seen in COVID-19 Patients Hint at Early Bone Marrow Reprogramming!
The research was conducted by scientists from Université de Lille, INSERM, CHU Lille (including the INFINITE and CIIL research centers), University of Wisconsin-Madison School of Medicine and Public Health, and France’s CEREO National Reference Center for Hypereosinophilic Syndromes.
Unlike previous studies that only looked at immune cells at a single timepoint, this
Medical News report reveals a more detailed and time-sensitive view of how three key immune cells—eosinophils, neutrophils, and monocytes—change their numbers and behavior during COVID-19.
Eosinophils Disappear Early but Show Signs of Mysterious Activation
One of the study’s most striking findings was the dramatic drop in eosinophils—white blood cells usually involved in allergy and parasite defense—within the first few days of hospitalization. These cells almost vanished from the bloodstream but showed signs of being highly activated. Scientists detected high levels of markers like CD69, CD63, and CD125 on the few eosinophils that remained. Interestingly, these cells also had low levels of other important markers such as CCR3 and CD44, which are usually involved in cell migration and communication.
This strange combination of markers doesn’t match any known state of mature or tissue-based eosinophils. The researchers believe this may be evidence that eosinophils are being reprogrammed right from their birth in the bone marrow before entering the bloodstream—something never seen before in COVID-19 or other viral infections. They also noted that the drop in eosinophils was not directly caused by typical signals like IL-5 or eotaxins in the blood, which usually guide eosinophils toward tissues.
Neutrophils Rise Later but Carry Dangerous Traits
While eosinophils dropped early, neutrophils—the most abundant white blood cells in the body—started increasing a few days into hospitalization. These cells were found in an unusual immature and hyperactivated state. The study found high numbers of neutrophils with low levels of CD10 (a maturity marker) and high levels of CD177, CD11b, and CD62L, all of which suggest that these cells could be involved in excessive inflammation.
Some of these neutrophils were likely contributing to NETosis—a process where neutrophils release web-like structures that trap pathogens but can also damage the lungs and contribute
to blood clots. The blood of patients showed elevated levels of proteins like MMP8, lactoferrin, and MPO, which are typically released by overactive neutrophils. These signs of neutrophil dysfunction remained for weeks, hinting at long-lasting immune damage in severe COVID-19 cases.
Monocytes Also Act Up Early Showing Proinflammatory Features
Monocytes, another type of white blood cell involved in the body’s first line of defense, were also found to be acting abnormally early in COVID-19. Patients showed lower monocyte counts on the first day of hospitalization, but the remaining cells displayed high levels of markers such as CD64, CD16, and IFNAR2. These are typically seen in inflammatory states and suggest the monocytes were highly activated and ready to interact with antibodies and interferons.
Additionally, CD163—a marker of monocyte activation—and CD32 were increased, while HLA-DR, a molecule important for signaling to other immune cells, was reduced. This combination of changes points to a dysfunctional immune response and supports earlier findings that overly activated monocytes might contribute to lung damage and worsen outcomes in COVID-19.
Chemicals in the Blood Support the Story
To better understand what might be triggering these immune cell changes, researchers also measured various cytokines and chemokines—chemical messengers that guide immune responses. They found that signals like IL-13 and eotaxin-2 (important in allergic responses and eosinophil movement) rose at specific times, though not in a pattern that fully explained the eosinophil drop.
In contrast, many markers of neutrophil activation and recruitment—including CXCL1, CXCL2, lipocalin-2, and proteinase 3—were consistently elevated, indicating a strong and sustained inflammatory reaction. For monocytes, the researchers observed elevated CX3CL1 early on, which is known to attract a type of monocyte linked to inflammation.
A New Way to Look at COVID Immune Damage
The research offers a new lens on how COVID-19 disrupts the immune system—not just by making immune cells overreact, but possibly by changing how they develop in the bone marrow. The findings suggest that eosinophils, neutrophils, and monocytes may all be recruited into tissues like the lungs at different times, potentially worsening inflammation or failing to control the virus effectively.
The researchers say more studies are needed to determine whether these immune cell shifts are unique to COVID-19 or also occur in other severe respiratory infections. They also note that tracking how immune cell types evolve over time in individual patients could help doctors predict disease severity or develop new treatments that target these dysfunctional immune pathways.
Conclusions
This study sheds light on the deeply disordered immune responses seen in severe COVID-19 cases, especially involving the earliest blood immune cells. The dramatic drop in eosinophils and the simultaneous rise of neutrophils and activated monocytes suggest a chaotic immune landscape that begins very early in the disease. The discovery that eosinophils may be undergoing a unique reprogramming in the bone marrow opens the door to new research into viral immunity. Understanding these processes could help us develop better treatments to stop the immune system from doing more harm than good in future outbreaks.
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.preprints.org/manuscript/202505.1163/v1
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