| First Author | Ding A | Year | 2005 |
| Journal | Immunology | Volume | 116 |
| Issue | 3 | Pages | 381-9 |
| PubMed ID | 16236128 | Mgi Jnum | J:103462 |
| Mgi Id | MGI:3609528 | Doi | 10.1111/j.1365-2567.2005.02238.x |
| Citation | Ding A, et al. (2005) Induction of macrophage-derived SLPI by Mycobacterium tuberculosis depends on TLR2 but not MyD88. Immunology 116(3):381-9 |
| abstractText | Macrophages respond to Mycobacterium tuberculosis by regulating expression of gene products that initiate a host innate response to this micro-organism. In this study, we report that exposure of murine peritoneal macrophages to heat-killed Mycobacterium tuberculosis (HK-Mtb) led to an increase in secretory leucocyte protease inhibitor (SLPI) gene expression and protein secretion in a time- and dose-dependent manner. HK-Mtb-induced SLPI mRNA expression was sensitive neither to a protein synthesis inhibitor, cycloheximide, nor to an actin polymerization blocker, cytochalasin D. Treatment of macrophages with interferon (IFN)-gamma inhibited HK-Mtb-induced SLPI expression. RAW264.7 cells stably expressing SLPI produced a reduced level of tumour necrosis factor (TNF) in response to HK-Mtb as compared with mock transfectants. Aerosol infection of mice with live M. tuberculosis resulted in an induction of SLPI gene expression in infected lungs. Macrophages from Toll-like receptor 4 (TLR4)-/- or MyD88-/- mice responded to M. tuberculosis similarly to wild-type macrophages by exhibiting increased SLPI expression. In contrast, macrophages from TLR2-/- mice were incapable of inducing SLPI in response to M. tuberculosis. This induction signifies the presence of a TLR2-dependent but MyD88-independent M. tuberculosis signalling pathway, suggesting involvement of adaptor protein(s) other than MyD88 in M. tuberculosis-mediated induction of SLPI. |
