Bastiani Michele, Vidotto Marilda Carlos, Horn Fabiana
Departamento de Biofísica, Universidade Federal do Rio Grande do Sul, P.O. Box 15005, 91501-970 Porto Alegre, RS, Brazil.
FEMS Microbiol Lett. 2005 Dec 1;253(1):133-40. doi: 10.1016/j.femsle.2005.09.024. Epub 2005 Oct 5.
Avian pathogenic Escherichia coli (APEC) strains, the etiological agent of colibacillosis in poultry, must resist the attack of incoming macrophages in order to cause disease. In this work, we show that an APEC strain (APEC17) remained viable inside J774 macrophages for at least 8 h and was cytotoxic to them 6-8 h after infection. APEC17 induced caspase 3/7 activation, the central caspases in apoptosis, in infected macrophages already at 2h after infection. Both cytotoxicity and caspase 3/7 activation were reduced when cells were infected with heat-killed APEC17, showing that bacteria must be viable to induce apoptosis. Our findings using APEC17 suggest that APEC may escape destruction by triggering macrophage apoptotic death.