Key result
Inflammatory myocarditis is linked to absent interleukin-1-receptor mRNA, suggesting disease-specific downregulation.
Why the study?
Diminished cardiac contractility associated with inflammatory infiltration may be mediated by interleukin release, but the presence of interleukin and interleukin-receptor mRNAs in human heart tissue was unclear.
Observational
Does not alter myocarditis management; hypothesis-generating for IL-1 receptor down-regulation in inflammatory cardiomyopathy.
Diminished cardiac contractility associated with inflammatory infiltration may be mediated by the release of interleukins. To test this hypothesis, we assessed the presence of interleukin and interleukin-receptor mRNAs in non-failing human heart and in endomyocardial biopsies from patients with dilated cardiomyopathy or inflammatory myocarditis. Only those interleukins expressed by non-circulating cells (interleukin-1 beta, -4, and -8) were detected in samples of human heart while interleukins specific for activated leukocytes (interleukins-1 alpha and -2) were not detected in any samples. While interleukin-1-receptor mRNA was present in samples from non-failing hearts and those with idiopathic myopathy, it was absent from patients with inflammatory myocarditis, suggesting receptor mRNA down-regulation.
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Han et al. (1991) conducted an observational in Dilated cardiomyopathy and inflammatory myocarditis. Dilated cardiomyopathy or inflammatory myocarditis vs. Non-failing human heart was evaluated on Presence of interleukin and interleukin-receptor mRNAs. Interleukin-1-receptor mRNA was present in non-failing hearts and idiopathic myopathy but absent in inflammatory myocarditis, suggesting receptor mRNA down-regulation.
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