Maoto is a widely used traditional Japanese medicine (Kampo) for upper respiratory tract infections, including influenza virus infection. In our previous study, we showed that maoto has ameliorative effects on the PolyI:C (Toll-like receptor 3 ligand)-induced acute inflammatory response and flu-like symptoms. Here, we investigated the involvement of immune responses and catecholamine-associated pathways in the inhibitory action of maoto.
In mice, oral maoto (2 g/kg) was administered in conjunction with intraperitoneal PolyI:C (6 mg/kg), and blood was collected 2 hours later. Plasma cytokine levels were measured by ELISA. Maoto significantly decreased the production of PolyI:C-induced TNF-a and increased the production of IL-10 as compared with mice given PolyI:C alone. Treatment with IL-10-neutralizing antibodies did not affect the inhibitory effect of maoto, and polyI:C-induced TNF-a production was also significantly suppressed by maoto in nude (T-cell-deficient) mice, indicating that the anti-inflammatory effect of maoto is independent of both IL-10- and T cells. Furthermore, we did not observe the inhibitory effect of maoto on PolyI:C-induced TNF-a production in inflammatory cells ex vivo. Collectively, these results suggest that the anti-inflammatory effect of maoto might be mediated by the systemic regulation of endogenous factors in vivo, and we are currently analyzing the involvement of adrenergic receptors and the sympathetic nervous system.