The effect of trehalose for the allergen-induced airway hyperresponsiveness and airway inflamation in mice

Background: Trehalose is a unique sugar and reported to inhibit the inflammatory cascade that in turn causes oxidative damage and cytokines production. In experimental septic shock, trehalose has been shown to inhibit proinflammatory phenotype activation in macrophages and prevent mortality. Aims: We investigated the potentials of trehalose to regulate the development of allergen-induced airway hypperresponsiveness (AHR) and airway inflamation. Methods: BALB/c mice were sensitized (days 0 and 14) and challenged (days 28-30) with ovalbumin (OVA). 2% trehalose was added to the water which the mice spontaneously drank from day -7 to day 32. Airway responses were monitored 48 hours after the last OVA-challenge (day 32). Lungs sections were stained with hematoxylin-eosin and periodic acid–Schiff (PAS) for identification of mucus-containing cells and examined. Oxidative stress was assessed by free radical analytical system (FRAS4). Results: Oral administration of trehalose significantly suppressed the development of AHR and eosinophilic infiltration in the airway. Trehalose attenuated the levels of IL-4, IL-5 and IL-13 in bronchoalveolar lavage fluid of the mice. Trehalose reduced the numbers of PAS positive cells. Trehalose increased the level of Biological Anti-oxidant Potential (BAP), and suppressed the levels of derivatives of Reactive Oxygen Metabolites (d-ROMs).Conclusions: These data suggest that trehalose may have a suppressive effect for the development of allergen-induced AHR, goblet cell metaplasia, and Th2-type cytokine production in the airway, which is associated with the suppression of oxidant stress, in a murine model of asthma.