| First Author | Hardison SE | Year | 2010 |
| Journal | Infect Immun | Volume | 78 |
| Issue | 12 | Pages | 5341-51 |
| PubMed ID | 20921149 | Mgi Jnum | J:166071 |
| Mgi Id | MGI:4839676 | Doi | 10.1128/IAI.00845-10 |
| Citation | Hardison SE, et al. (2010) Interleukin-17 Is Not Required for Classical Macrophage Activation in a Pulmonary Mouse Model of Cryptococcus neoformans Infection. Infect Immun 78(12):5341-51 |
| abstractText | Cryptococcus neoformans is an opportunistic fungal pathogen that causes disease in individuals with suppressed cell-mediated immunity. Recent studies in our laboratory have shown that increases in pulmonary Th1-type and interleukin-17A (IL-17A) cytokine production, classical macrophage activation, and sterilizing immunity are elicited in response to infection with a gamma interferon (IFN-gamma)-producing C. neoformans strain, H99gamma. IL-17A-treated macrophages, compared to IL-4-treated macrophages, have been demonstrated to exhibit increased microbicidal activity in vitro, a characteristic consistent with classical macrophage activation. The purpose of these studies is to determine the role of IL-17A in the induction of classically activated macrophages following infection with C. neoformans. Immunohistochemistry and real-time PCR were used to characterize the macrophage activation phenotype in lung tissues of mice treated with isotype control or anti-IL-17A antibodies and given an experimental pulmonary infection with C. neoformans strain H99gamma. The pulmonary fungal burden was resolved, albeit more slowly, in mice depleted of IL-17A compared to the fungal burden in isotype control-treated mice. Nonetheless, no difference in classical macrophage activation was observed in IL-17A-depleted mice. Similarly, classical macrophage activation was evident in mice deficient in IL-17A or the IL-17 receptor A, which mediates IL-17A signaling, following pulmonary infection with wild-type C. neoformans strain H99 or H99gamma. These studies suggest that IL-17A may play a role in the early immune response to C. neoformans but is not required for classical macrophage activation in mice experimentally infected with C. neoformans. |
