Open AccessAn avian pathogenic Escherichia coli isolate induces caspase 3/7 activation in J774 macrophages
Author(s) -
Bastiani Michele,
Vidotto Marilda Carlos,
Horn Fabiana
Publication year - 2005
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1016/j.femsle.2005.09.024
Subject(s) - microbiology and biotechnology , escherichia coli , pathogenic escherichia coli , apoptosis , macrophage , cytotoxic t cell , biology , caspase , bacteria , cytotoxicity , strain (injury) , pathogenic bacteria , programmed cell death , in vitro , biochemistry , gene , genetics , anatomy
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 2 h 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.