Mycobacterium avium complex (MAC) is the most common cause of nontuberculous mycobacterial disease in humans. The role of Th17 immunity in the pathogenesis of intracellular bacteria, such as MAC, is not currently understood. Transcription factor RAR-related orphan receptor gamma t (ROR[gamma]t) is known as the master regulator for Th17 cell development. Here, we investigated the role of ROR[gamma]t in host responses against MAC infection. Wild-type (WT) mice and ROR[gamma]t-overexpressing mice were infected with MAC via intratracheal inoculation. Systemic MAC growth was not different between WT mice and ROR[gamma]t-overexpressing mice. However, neutrophilic pulmonary inflammation following MAC infection was enhanced in ROR[gamma]t-overexpressing mice compared with that in WT mice. The cytokine expression shifted toward a Th17 phenotype in the lungs of ROR[gamma]t-overexpressing mice following MAC infection; the levels of IL-6 and IL-17 were significantly higher in the lung of these mice than in WT mice. In addition to the increase in IL-17 single-positive T cells, T cells producing both IL-17 and interferon-[gamma] were elevated in the lung of ROR[gamma]t-overexpressing mice following MAC infection. These findings suggest that ROR[gamma]t overexpression-mediated Th17 bias contributes to local inflammation rather than systemic responses, by regulating neutrophil recruitment into the sites of infection during MAC infection.