Flesch I E, Kaufmann S H
Max-Planck-Institut für Immunbiologie, Freiburg, Federal Republic of Germany.
Infect Immun. 1988 Jun;56(6):1464-9. doi: 10.1128/iai.56.6.1464-1469.1988.
Bone marrow-derived murine macrophages are able to inhibit the growth of Mycobacterium bovis and of some strains of M. tuberculosis after stimulation with either recombinant gamma interferon (rIFN-gamma) or lymphokines from antigen-specific T-cell clones. To elucidate the mechanism(s) involved in antimycobacterial activity, macrophages were infected with M. bovis in the presence of agents thought to influence the antimicrobial effects of phagocytes. Scavengers of toxic oxygen metabolites failed to influence the capacity of IFN-gamma-activated bone marrow macrophages to inhibit the growth of M. bovis. Suramin slightly affected mycobacterial growth in IFN-gamma-activated macrophages, and chloroquine markedly induced growth inhibition of M. bovis in unstimulated macrophages. We conclude that growth inhibition of M. bovis by IFN-gamma-activated macrophages is an oxygen-independent process.
骨髓来源的小鼠巨噬细胞在用重组γ干扰素(rIFN-γ)或抗原特异性T细胞克隆产生的淋巴因子刺激后,能够抑制牛分枝杆菌和某些结核分枝杆菌菌株的生长。为了阐明参与抗分枝杆菌活性的机制,在存在被认为会影响吞噬细胞抗菌作用的试剂的情况下,用牛分枝杆菌感染巨噬细胞。有毒氧代谢产物的清除剂未能影响IFN-γ激活的骨髓巨噬细胞抑制牛分枝杆菌生长的能力。苏拉明对IFN-γ激活的巨噬细胞中的分枝杆菌生长有轻微影响,而氯喹显著诱导未刺激的巨噬细胞中牛分枝杆菌的生长抑制。我们得出结论,IFN-γ激活的巨噬细胞对牛分枝杆菌的生长抑制是一个不依赖氧的过程。