Interleukin-4 (IL-4) and Interleukin-13 (IL-13) inhibit IL-1β induction of Interleukin-8 (IL-8) and Epithelial neutrophil activating protein (ENA-78) in alveolar type II cells. 1958

Alveolar type II cells participate in inflammatory processes of the lung by elaborating chemotactic cytokines in response to IL-1β. Since IL-4, IL-13 and IL-10 have been shown to influence macrophage production of inflammatory cytokines, particularly IL-8, we assessed the ability of these cytokines to modify IL-1β induced chemokine release in type II cells. A549 cells were incubated with 100 ng/ml of IL-4,10 and 13 for 24 hours prior to the addition of 50 pg /ml IL-1β. Culture supernatants were examined for IL-8, MCP-1 and ENA-78 after 24 hours incubation. Interleukin-4 and IL-13 significantly inhibited IL-1β induced IL-8 and ENA-78 production. Interleukins 4, 10 and 13 (100 ng/ml) alone had no effect on IL-8 or ENA-78 production. Our results suggest that IL-4 and IL-13 may regulate chemokine production in alveolar type II cells. In contrast to its effects in macrophages, IL-10 has little effect on IL-8, MCP-1 or ENA-78 production in type II cells. Data represent Mean±SE of 7 experiments.(*p<0.05;^#p=0.06) Table

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