Why the study?
The response of the immune system to recurrent cardiac tissue injury, and whether adaptations lead to immune cell hypo-responsiveness or hyper-responsiveness, is not well understood.
Initial adrenergic-mediated cardiac injury induces a macrophage-dependent disease tolerance that protects the heart from subsequent stress-induced cardiomyopathy.
Hypothesis-generating for macrophage-mediated tolerance after adrenergic injury in rodents; leaves open translation to human stress cardiomyopathy.
Whereas the innate immune response to an initial episode of cardiac injury has been studied extensively, the response of the immune system to recurrent cardiac tissue injury is not well understood. Specifically, it is not known whether the immune system adapts to the initial episode of cardiac injury and whether any adaptations that occur lead to immune cell hypo-responsiveness or, alternatively, immune cell hyper-responsiveness. Here, we studied the role of adrenergic-mediated stress using a simple model of reversible stress-induced cardiomyopathy, and show that isoproterenol-induced tissue injury and inflammation are sufficient to protect the heart from the myopathic effects of a subsequent exposure to isoproterenol. Remarkably, pharmacological depletion of macrophages partially attenuated the isoproterenol-induced cytoprotective response, suggesting that immune-mediated tissue repair mechanisms confer tolerance to subsequent tissue damage.
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Tiwary et al. (2023) studied this question.
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