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Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction

Joseph J Sepe1,2, Ryan T Gardner1,2, Matthew R Blake1

  • 1Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, USA.

JACC. Basic to Translational Science
|November 1, 2022
PubMed

Myocardial infarction (MI) triggers an inflammatory response that transitions from pro-inflammatory to reparative over time. Restoring sympathetic nerves in the heart after MI prevents arrhythmias. This study investigated if reinnervation altered the immune response after MI. This study used quantitative multiplex immunohistochemistry to identify the immune cells present in the heart 2 weeks after ischemia-reperfusion. Two therapeutics stimulated reinnervation, preventing arrhythmias and shifting the immune response from inflammatory to reparative, with fewer pro-inflammatory macrophages and more regulatory T cells and reparative macrophages. Treatments did not alter macrophage phenotype in vitro, which suggested reinnervation contributed to the altered immune response.

Keywords:
ACh, acetylcholineIP, intraperitonealISP, intracellular sigma peptideMI, myocardial infarctionNE, norepinephrinePBS, phosphate-buffered salineTH, tyrosine hydroxylaseTregs, regulatory T cellsVEH, vehicleinflammationmIHC, multiplex immunohistochemistrymacrophagesmultiplex IHCmyocardial infarctionsympathetic nervous systemβ1-AR, adrenergic receptor

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