Immune Modulation by Catecholamines - a Potential Mechanism of Cytokine Release in Heart Failure?

Abstract

Cytokine blood levels are found to be moderately elevated in chronic heart failure, as a function of severity of disease. The source of these cytokines and the trigger mechanisms stimulating cytokine release are a matter of intense research. Potential players include bacterial endotoxin from intestinal translocation, a neurohumoral dysbalance with an enhanced sympathetic tone or an overspill of cytokines from the failing heart itself. We present arguments in favor of a direct link between the chronically enhanced sympathetic tone in heart failure and the clinically overt activation of the immune system, particularly interleukin 6 release.

Making the Case for Skeletal Myopathy as the Major Limitation of Exercise Capacity in Heart Failure

“…Ample evidence supports the concept that HF from systolic dysfunction leads to a systemic inflammatory response (30). This inflammation involves the skeletal musculature, and contributes importantly to the skeletal myopathy of heart failure (1–3,30–39).…”

Role of Exercise Training on Autonomic Changes and Inflammatory Profile Induced by Myocardial Infarction

“…There are at least five hypotheses addressing the underlying mechanism of inflammatory response [48]: (1) the failure of the myocardium per se would be the main source of cytokine production [49]; (2) the circulatory decompensation would lead to increased intestinal translocation of bacterial endotoxin (lipopolysaccharide) to the systemic circulation, which in turn would activate circulating immune cells [50]; (3) the main source of proinflammatory mediators would be the body tissues exposed to hypoxia [51, 52]; (4) immune activation would be a consequence of increased [53] sympathetic stimulation; and (5) reduction in parasympathetic participation would work as the primary mediator of the inflammatory response activation [48]. …”

The Gut and Intestinal Bacteria in Chronic Heart Failure

“…Indeed, the most relevant hypotheses [19] include local production by the myocardium itself [20] or by invaded proinflammatory cells [21], local secretion as a response to hypoxia [22], sympathetic or neurohormonal activation [23], central suppression of the parasympathetic nervous system [24] and lipopolysaccharide (LPS, otherwise known as endotoxin) triggered cytokine release [2]. Indeed, very small, i.e.…”