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Viral infections play an important role in the exacerbation of asthma. The production of interferons (IFNs) is well known to limit viral spread, but IFN-γ can also prime alveolar macrophages to release more inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein-1α (MIP-1α). Given the importance of these cytokines, we have investigated the effect of IFN-γ on their release by alveolar macrophages during stimulation by immunoglobulin (Ig)E/anti-IgE. Alveolar macrophages from normal or Nippostrongylus brasiliensis-infected rats, the latter having increased numbers of low-affinity receptors for IgE (Fcε RII) on their alveolar macrophages, were treated with IgE for 2 h and stimulated with anti-IgE for 18 h. The increase of TNF-α release (153 ± 48 pg/106 cells) by IgE/anti-IgE occurred only with alveolar macrophages from infected rats. The messenger RNA level for TNF-α in rat alveolar macrophages was also increased by stimulation with IgE/anti-IgE. Treatment with IFN-γ prior to stimulation with IgE/anti-IgE showed a time- and concentration-dependent increase of TNF-α release. Interestingly, IgE/anti-IgE treatment did not stimulate the release of MIP-1α (15 ± 5 pg/106 cells), but IFN-γ treatment alone and with IgE /anti-IgE significantly increased and potentiated MIP-1α release (98 ± 40 pg/106 cells) by alveolar macrophages, respectively. These results suggest that IFN-γ produced at times such as during viral infections primes alveolar macrophages for enhanced release of inflammatory mediators during allergic reactions, thereby contributing to the inflammatory process.