PubMed · 14945967
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C M RILEY. 1952-08-23. Familial autonomic dysfunction.. https://doi.org/10.1001/jama.1952.02930340016006
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Type I interferons (IFN-alpha and -beta) play a key role in anti-viral immunity, and we sought to define the molecular mechanisms by which the sympathetic nervous system (SNS) inhibits their effects. In peripheral blood leukocytes and plasmacytoid dendritic cells (pDC2), induction of interferon anti-viral activity by double-stranded RNA (poly-I:C) or CpG DNA was substantially inhibited by norepinephrine and by pharmacologic activation of the cAMP/PKA signaling pathway. This effect was specific to Type I interferons and driven by PKA-mediated repression of IFNA and IFNB gene transcription. Luciferase reporter analyses identified tandem interferon response factor-binding sites in positive regulatory domains I and III of the IFNB promoter as a key target of PKA inhibition. PKA suppression of Type I interferons was associated with impaired transcription of interferon response genes supporting the "anti-viral state", and was sufficient to account for norepinephrine-induced enhancement of HIV-1 replication. Given the ubiquitous role of Type I interferons in containing viral replication, PKA-mediated inhibition of IFN transcription could explain the stimulatory effects of catecholamines on a broad range of viral pathogens.
Activation of the immune system and derangement of cardiorespiratory neural control are established elements of the complex pathophysiology of chronic heart failure (CHF). The magnitude of these abnormalities relates to disease progression and mortality. Less clear is the origin of these derangements and the sequence of triggering mechanisms in the course of the natural history of CHF. To date, immune activation and autonomic imbalance have been considered independently; we hypothesise they are closely related. Damaged heart muscle through autonomic afferents triggers functional and structural changes in the central nervous system, in part related to inflammatory processes. The altered function of the autonomic centres is expressed as a reduction of central parasympathetic tone. Diminished cholinergic signalling (mainly nicotinergic) activates inflammation and stimulates immune response. These two phenomena predict prognosis and represent therapeutic targets in the syndrome of CHF.
The incidence of cardiovascular disease is higher in postmenopausal women than in premenopausal women. We hypothesized that long-term vegetarian diets might modulate cardiovascular autonomic functions measured by frequency-domain techniques in healthy postmenopausal women. A total of 35 healthy vegetarians (mean age +/- SEM 55.0 +/- 1.3 years) who had been vegetarians for > or =2 years and 35 omnivores (55.1 +/- 1.4 years) participated in this study. These subjects were all postmenopausal without hormone replacement therapy. Fluctuations in arterial blood pressure and heart rate variability were diffracted into low-frequency (0.04 to 0.15 Hz) and high-frequency (0.15 to 0.4 Hz) segments. Cardiovascular autonomic functions and baroreflex sensitivity were evaluated by specific frequency-domain measures. The vegetarians had statistically lower systolic and diastolic blood pressure, and lower serum total cholesterol, low-density lipoprotein cholesterol, triglycerides, fasting blood sugar, and hemoglobin levels compared with the nonvegetarians. They also exhibited a significantly higher high-frequency power of heart rate variability and increased baroreflex sensitivity than did omnivores. No statistical differences were found in the low-frequency/high-frequency ratio or percentage of low frequency of heart rate variability between the 2 groups. In conclusion, in addition to the lower blood pressure and lipid concentrations in vegetarians, long-term vegetarian diets may facilitate vagal regulation of the heart and increase baroreflex sensitivity in healthy postmenopausal women, without increasing the sympathetic modulations of the cardiovascular system.