| First Author | Eitel J | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 1 | Pages | e30379 |
| PubMed ID | 22276187 | Mgi Jnum | J:224064 |
| Mgi Id | MGI:5661151 | Doi | 10.1371/journal.pone.0030379 |
| Citation | Eitel J, et al. (2012) Rac1 regulates the NLRP3 inflammasome which mediates IL-1beta production in Chlamydophila pneumoniae infected human mononuclear cells. PLoS One 7(1):e30379 |
| abstractText | Chlamydophila pneumoniae causes acute respiratory tract infections and has been associated with development of asthma and atherosclerosis. The production of IL-1beta, a key mediator of acute and chronic inflammation, is regulated on a transcriptional level and additionally on a posttranslational level by inflammasomes. In the present study we show that C. pneumoniae-infected human mononuclear cells produce IL-1beta protein depending on an inflammasome consisting of NLRP3, the adapter protein ASC and caspase-1. We further found that the small GTPase Rac1 is activated in C. pneumoniae-infected cells. Importantly, studies with specific inhibitors as well as siRNA show that Rac1 regulates inflammasome activation in C. pneumoniae-infected cells. In conclusion, C. pneumoniae infection of mononuclear cells stimulates IL-1beta production dependent on a NLRP3 inflammasome-mediated processing of proIL-1beta which is controlled by Rac1. |
