Researchers from Yale School of Medicine devised an innovative method for reducing heart muscle damage caused by neutrophil activation during myocardial infarction. As part of this study, a technique was proposed to shift these immune cells into a state akin to their “night mode.” The work’s findings are reported in the esteemed journal, Journal of Experimental Medicine.
Neutrophils are central effector cells in innate immunity, becoming activated in response to tissue injury and pathogenic agents. They serve a vital purpose in phagocytosis and tissue repair processes. However, during chronic inflammation or ischemic damage to the myocardium, neutrophils can display cytotoxic activity, releasing proinflammatory mediators and enzymes that facilitate the destruction of healthy tissues.
It is recognized that neutrophils exhibit a daily cycle of activity, with peak functional expression during daytime hours and reduced activity during the night. This circadian pattern may account for the worse prognosis in patients who experience myocardial infarction in the morning hours, when the level of neutrophilic aggression is highest.
During the experiment, investigators employed the drug ATI2341 in a myocardial infarction model using mice. This pharmacological agent specifically interacts with receptors on the neutrophil surface, prompting their transition into a state of diminished functional activity, similar to their “night setting.” Administering ATI2341 to mice with experimental myocardial infarction resulted in a substantial decrease in the extent of cardiac tissue damage and an improvement in its functional capacity. Neutrophils maintained their presence in the area of ischemic injury, lessening the danger of harm to surrounding tissues, while their overall immune reaction to pathogens remained intact.
Professor Andrés Hidalgo remarked that this approach constitutes a promising strategy for safely managing the inflammatory response following myocardial infarction. This discovery opens new avenues for creating pharmacological agents aimed at safeguarding the myocardium without adversely affecting the body’s general immune function. Despite the need for further clinical trials to assess the method’s efficacy and safety in humans, the preliminary outcomes indicate its considerable promise.
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