Inflammation in asthma is characterized by a Th2 response. In many experimental systems, this response can be regulated by interleukin (IL)-10 and IL-12. IL-10 deactivates T cells, and IL-12 reorients the response toward a Th1 pattern. Alveolar macrophages (AM) can secrete both of these cytokines, and thus regulate T-cell behavior in asthma. They can enhance the Th2 response by turning off their secretion of IL-10 and IL-12, or tend to downregulate it by producing these cytokines. To elucidate that point, we assayed the AM IL-10 and IL-12 from 11 asthmatic patients and four controls. Six asthmatics were treated by inhaled corticosteroids. AM were recovered by bronchoalveolar lavage (BAL). They were isolated and cultured for 24 h without stimulation or in the presence of lipopolysaccharide (LPS). IL-10 and the p40 subunit of IL-12 were assayed in the BAL fluid and in AM culture supernatants by ELISA. Spontaneous AM IL-10 production was higher in asthmatics, particularly in the treated group. The AM IL-10 production after stimulation by LPS was also elevated in asthmatics, but was mainly so in untreated patients. IL-12 levels were higher in BAL fluids from untreated patients than from controls. The IL-12 production of LPS-stimulated-AM from these patients was increased. These results show that AM are at least primed for the production of IL-10 and IL-12 in asthma, and suggest that these cells could be involved in the resolution of the asthmatic inflammation.