Catecholamines increase monocyte TNF receptors and inhibit TNF through β₂-adrenoreceptor activation

Abstract

Postinjury deficits in monocyte tumor necrosis factor receptors (moTNFR) activity may alter beneficial functions during an inflammatory response. Several counter-regulatory hormones elicited during inflammation may modulate tumor necrosis factor (TNF) activity, but little is known about their influence on moTNFR. Also, catecholamines inhibit TNF production, but the adrenoreceptor mechanism of this effect has not been fully clarified. To determine the effect of catecholamines and corticosteroids on moTNFR, whole blood was coincubated for up to 8 (moTNFR) or 24 h (cytokines) in the presence of lipopolysaccharide (100 ng/ml) and 1) epinephrine (Epi, 10−6 M), dexamethasone (Dex, 10−6 M) or both (EpiDex, 10−6 M) to assess the expression of total moTNFR, moTNFR-I, and moTNFR-II. 2) Epi and norepinephrine (EpiNE, 10−6 M) and the α1+2-, β1+2-, β1-, or β2-adrenergic antagonists were used to assess the role of such adrenoreceptors on total moTNFR and TNF production, and N 6,2′- O-dibutyryl adenosine 3′,5′-cyclic monophosphate (DBcAMP) alone or in combination with the phosphodiesterase inhibitor Ro-20–1724/000, to study the cAMP-dependent pathway on total moTNFR. We found that Epi upregulated total moTNFR and moTNFR-II. Dex did not significantly influence total moTNFR or moTNFR-II. Also, EpiNE increased total moTNFR and inhibited TNF by a β2-dependent mechanism. DBcAMP (10−5 M) modestly enhanced total moTNFR. This suggests a common mechanism for acutely enhancing moTNFR and attenuation of soluble TNF appearance during conditions of severe stress.

Propranolol ameliorates and epinephrine exacerbates progression of acute and chronic viral myocarditis

“…Catecholamines act through ␤-adrenergic receptors to regulate the expression of the cytokine receptors (8). Epinephrine and norepinephrine have immunosuppressive effects (13).…”

Do Resistin and Tumor Necrosis Factor-α Relate to Changes in Insulin Resistance in Normal Pregnancy?

“…In addition pregnancy to be associated with changes of several hormones, including, estrogen, progesterone, cortisol and 1, 25 dihydroxyvitamin D3 (Henricks et al, 1972;Smith et al, 1973;Ardawi et al, 1997). Some of these hormones such as cortisol and catecholamines and 1, 25 dihydroxy D3 are potent inhibitor of TNF-α production by monocyte/macrophage (DeRijk et al, 1997;Guirao et al, 1997;Anand et al, 2009;Ito et al, 2002). In other study has been shown, plasma concentration of cortisol was elevated more during late pregnancy than early pregnancy (Kirwan et al, 2002).…”

Physiological regulation of pro-inflammatory cytokines expression in rat cardiovascular tissues by sympathetic nervous system and angiotensin II

“…In contrast, enhanced cytokine production was associated with hyperactivity of SNS (Petretta et al 2000) and high plasma norepinephrine levels (Kinugawa et al 2003). Furthermore, it has been shown in vivo and in vitro that cytokine production by the heart may be regulated by SNS through β-adrenergic receptors (Guirao et al 1997;Kan et al 1999;Prabhu et al 2000). Chronic β-adrenergic stimulation with isoproterenol enhances gene expression and protein production of TNF-α, IL-1 β, and IL-6 in the heart while β-adrenergic receptors antagonists inhibit these productions (Kan et al 1999).…”