Abstract
We have previously reported that low-grade systemic inflammation is associated with compromised immunocompetence in obese individuals. We then showed that an extended recombinant human-TNF treatment of monocytes results in decreased immune response, indicating contribution of chronic inflammation in compromised immunity in obesity. In this study we aimed to further investigate a cellular mechanism of obesity-related inflammation. We hypothesized that the responsivity of monocytes’ beta2 adrenergic ( beta 2-ARs) and glucocorticoid receptors (GR) to agonists is impaired among the obese. beta 2-AR and GR responsivity was examined by assessing intracellular TNF expression in monocytes upon ex vivo LPS-stimulation by flow cytometry with and without isoproterenol (Iso; 10 −10 –10 −8 M) and cortisol (0.1–1 μM), respectively. Plasma IL-1 beta , IL-6, TNF, and cortisol levels were determined by immunoassay. Ninety-six asymptomatic individuals participated, and the associations among depressive mood, obesity, and GR responsivity were investigated in a subset ( N = 35). Beta 2-AR responsivity to Iso in TNF inhibition was smaller among the obese compared to lean individuals ( p ’s beta 2-AR responsivity was negatively associated with plasma levels of IL-1 beta , IL-6 and TNF ( p ’s p ’s
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