| First Author | Pizarro-Cerdá J | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 6 | Pages | 3519-26 |
| PubMed ID | 10092809 | Mgi Jnum | J:53457 |
| Mgi Id | MGI:1332746 | Doi | 10.4049/jimmunol.162.6.3519 |
| Citation | Pizarro-Cerda J, et al. (1999) Modulation of endocytosis in nuclear factor IL-6(-/-) macrophages is responsible for a high susceptibility to intracellular bacterial infection. J Immunol 162(6):3519-26 |
| abstractText | Activated macrophages kill bacteria, a function known to depend on the expression of NF-IL-6. Here, it is demonstrated that the attenuated Brucella abortus vaccine strain 19 replicates much better in NF-IL-6-/- than in NF-IL-6(+/+) and NF-IL-6(+/+)-activated murine macrophages and at levels comparable to those observed in normal macrophages infected with the pathogenic strain 2308. The role of NF-IL-6 in the inhibition of intracellular bacterial replication is related to its control of endocytosis and membrane fusion between endosomes and Brucella-containing phagosomes. Addition of the granulocyte-CSF (G-CSF), whose induction is impaired in NF-IL-6(-/-) macrophages, restores both endocytosis and the morphology of endosomes, together with bactericidal activity. Regulation of membrane traffic in endocytosis by G-CSF whose expression is controlled by NF-IL-6 may explain how a host cell can control intracellular bacterial replication. |
