Prednisone is a widely used corticosteroid medication prescribed for a variety of conditions involving inflammation. Neutrophils are a type of white blood cell that combats infections. The administration of prednisone has a well-documented and predictable effect on the number of neutrophils circulating in the bloodstream. This relationship is important for both patients and clinicians to understand, as it alters a common measure of immune system status.
The Role of Neutrophils in the Immune System
Neutrophils are the most common type of white blood cell and act as the immune system’s first responders. They are produced and mature within the bone marrow before being released into the bloodstream. Their primary purpose is to travel to sites of infection or tissue injury, where they work to eliminate invading pathogens like bacteria and fungi.
These cells have a short lifespan, circulating in the blood for about 6 to 8 hours before being cleared. This turnover requires the bone marrow to produce billions of new neutrophils daily to ensure a continuous supply is available.
A large portion of neutrophils in the bloodstream are not freely floating but exist in the “marginated pool.” These are cells that are temporarily adhered to the inner walls of small blood vessels, particularly in organs like the lungs, spleen, and liver. This population acts as a reserve that can quickly re-enter circulation when needed.
When neutrophils detect chemical signals from a site of injury or infection, they stick firmly to the vessel wall and squeeze through the lining to enter the affected tissue. Once in the tissue, they destroy pathogens through phagocytosis or by releasing antimicrobial substances.
How Prednisone Increases Neutrophil Count
Prednisone and other corticosteroids increase neutrophil counts through several biological mechanisms, leading to a higher number of these cells in blood samples. The most immediate effect is demargination, which is responsible for an estimated 60% of the increase. Prednisone reduces the expression of adhesion molecules on the neutrophil surface, making them less “sticky.” These molecules are what allow neutrophils to cling to the walls of blood vessels.
This reduced adhesion causes the release of the marginated pool of cells into the main circulation. A blood draw will then show a higher neutrophil count from this inflated circulating pool. This change occurs within a few hours of taking the medication.
Prednisone also accelerates the release of mature neutrophils from the bone marrow’s reserves. This mechanism contributes approximately 10% to the overall rise in neutrophil count.
A third action of prednisone is delaying apoptosis, or programmed cell death, in neutrophils. Prednisone allows them to survive and accumulate in the blood for longer periods. This extended survival, combined with demargination and increased bone marrow release, accounts for the remaining portion of the elevated count.
The Effect on Neutrophil Function
While prednisone increases the number of circulating neutrophils, it also impairs their function. This means a high neutrophil count on a lab report can mask a compromised immune defense. The same mechanism that causes demargination—the reduction of adhesion molecules—also hinders the neutrophils’ effectiveness.
To fight an infection, a neutrophil must leave the bloodstream and enter the affected tissue. This process, called extravasation, requires the cell to adhere to the blood vessel wall. Because prednisone makes neutrophils less sticky, it disrupts their ability to exit the circulation where they are needed. The cells are numerous in the blood but less able to reach the site of infection in the tissues.
This interference with migration is part of the anti-inflammatory effect of corticosteroids. By preventing neutrophils from congregating at a site of inflammation, prednisone can reduce swelling, redness, and pain. However, this action also weakens the body’s response to infections. The neutrophils are less able to perform chemotaxis, the process of moving toward chemical signals from pathogens.
A patient on prednisone therapy may have a high white blood cell count but is considered immunocompromised. The high count reflects a buildup of neutrophils in the bloodstream that cannot exit to sites of infection. This explains why individuals taking steroids are more susceptible to developing infections and may have a harder time clearing them, despite having an abundance of these “first responder” cells.
Clinical Interpretation of Prednisone-Induced Neutrophilia
An elevated neutrophil count, or neutrophilia, is an expected finding in patients taking prednisone, and the degree of increase is dependent on the steroid dose. The total white blood cell count can reach levels that might otherwise suggest an infection. This state is benign and reversible, with counts returning to normal after the steroid is stopped.
A doctor must distinguish this benign steroid-induced neutrophilia from neutrophilia caused by an infection. This relies on a broader clinical assessment, not just the neutrophil count. A patient with an infection presents with other signs like fever or localized pain, which are not caused by steroid effects alone.
Lab results provide more clues. During a bacterial infection, the body releases more immature neutrophils, known as “bands,” from the bone marrow. This “left shift” indicates the immune system is increasing production to fight a threat. Steroid-induced neutrophilia does not cause a significant left shift because it involves the release of mature cells.
Doctors may also check inflammatory markers like C-reactive protein (CRP), which is elevated during an infection but not necessarily from prednisone use alone. By considering the patient’s symptoms, the left shift, and other markers, clinicians can interpret a high neutrophil count in a patient on prednisone as a physiological response to the medication, not a sign of infection.