Interaction between nutrition and production of IL-1 beta, TNF alpha, and IL-6 by peripheral blood monocytes in patients with lung cancer

Abstract

Altered nutrient intake and metabolism are responsible for the progressive loss of body weight observed in most patients with advanced cancer, but the precise mechanism is still controversial. Under stressful conditions, some inflammatory cytokines such as IL-1 beta, TNF alpha, and IL-6 have a hypermetabolic effect and cause proteolysis and lipolysis in muscle and in fat tissues. To elucidate the mechanism of malnutrition in patients with lung cancer and normal food intake, we focused on the relationship between abnormal metabolism and these inflammatory cytokines. Patients with lung cancer were confirmed to be malnourished, and this malnutrition was found to be caused by hypermetabolism as estimated with visceral proteins, plasma levels of amino acids, and anthropometric indices. The production of IL-1 beta, TNF alpha, and IL-6 by blood monocytes was significantly higher in these patients than in healthy controls, and it correlated significantly and inversely with indices of nutrition. The present results suggest that nutritional status and these cytokines are closely related in patients with lung cancer. IL-1 beta, TNF-alpha, and IL-6 may serve as anti-cancer bioactive molecules, but "overfunctioning" of these cytokines may induce a hypermetabolic status that causes malnutrition, i.e. cancer cachexia.