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      Beta Blocker and Angiotensin-Converting Enzyme Inhibitor Therapy Is Associated with Decreased Th1/Th2 Cytokine Ratios and Inflammatory Cytokine Production in Patients with Chronic Heart Failure

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          Objective: To examine the potential impact of β-blockers and angiotensin-converting enzyme (ACE) inhibitors, medications which modulate β-adrenergic signaling, on immune function in patients with chronic heart failure (HF). Methods: 118 patients attending an HF center were tested for circulating levels of norepinephrine (NE), T cells and the inflammation-associated cytokine interleukin 6 (IL-6). Levels of the cytokines interferon-γ (IFNγ), IL-10, and tumor necrosis factor-α (TNFα) produced by cultured peripheral blood mononuclear cells (PBMC) were measured in culture supernatants following T cell stimulation in vitro. Results: NE levels were significantly lower in patients receiving ACE inhibitors (p = 0.0263), with a trend toward lower NE in patients receiving β-blockers. All patients exhibited relatively normal levels of T cells, and there was a trend toward higher levels of total (CD3+) and helper (CD4+) T cells (p = 0.0578 and 0.0932, respectively) in patients receiving either type of medication. The ratios of Th1 (IFNγ) to Th2 (IL-10) cytokines were lower in patients receiving a combination of β-blocker and ACE inhibitor therapy (p = 0.0373). NYHA class was a significant predictor of serum IL-6 (p < 0.0001). There was a trend toward lower levels of serum IL-6 in patients receiving both types of medications (p = 0.0606). TNFα production by CD3/CD28-stimulated PBMC was significantly lower in patients receiving ACE inhibitor medications (p = 0.0223). Conclusions: These results suggest that high sympathetic tone associated with chronic HF affects Th1/Th2 and inflammatory cytokine production, and that these effects can be modulated by medications. In addition to improvement in clinical parameters relating to cardiovascular function, β-blocker and ACE inhibitor medications also appear to have a beneficial effect on the immune system in HF.

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          Most cited references 18

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          Stress and the inflammatory response: a review of neurogenic inflammation.

           Paul H. Black (2002)
          The subject of neuroinflammation is reviewed. In response to psychological stress or certain physical stressors, an inflammatory process may occur by release of neuropeptides, especially Substance P (SP), or other inflammatory mediators, from sensory nerves and the activation of mast cells or other inflammatory cells. Central neuropeptides, particularly corticosteroid releasing factor (CRF), and perhaps SP as well, initiate a systemic stress response by activation of neuroendocrinological pathways such as the sympathetic nervous system, hypothalamic pituitary axis, and the renin angiotensin system, with the release of the stress hormones (i.e., catecholamines, corticosteroids, growth hormone, glucagons, and renin). These, together with cytokines induced by stress, initiate the acute phase response (APR) and the induction of acute phase proteins, essential mediators of inflammation. Central nervous system norepinephrine may also induce the APR perhaps by macrophage activation and cytokine release. The increase in lipids with stress may also be a factor in macrophage activation, as may lipopolysaccharide which, I postulate, induces cytokines from hepatic Kupffer cells, subsequent to an enhanced absorption from the gastrointestinal tract during psychologic stress. The brain may initiate or inhibit the inflammatory process. The inflammatory response is contained within the psychological stress response which evolved later. Moreover, the same neuropeptides (i.e., CRF and possibly SP as well) mediate both stress and inflammation. Cytokines evoked by either a stress or inflammatory response may utilize similar somatosensory pathways to signal the brain. Other instances whereby stress may induce inflammatory changes are reviewed. I postulate that repeated episodes of acute or chronic psychogenic stress may produce chronic inflammatory changes which may result in atherosclerosis in the arteries or chronic inflammatory changes in other organs as well.
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            Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients

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              Randomised trial of losartan versus captopril in patients over 65 with heart failure (Evaluation of Losartan in the Elderly Study, ELITE)


                Author and article information

                S. Karger AG
                April 2004
                14 April 2004
                : 11
                : 3
                : 173-180
                Departments of aObstetrics and Gynecology, bMedicine and cMicrobiology, Immunology and Molecular Genetics, David Geffen School of Medicine at UCLA and dUCLA School of Nursing, Los Angeles, Calif., USA
                76766 Neuroimmunomodulation 2004;11:173–180
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 46, Pages: 8
                Original Paper


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