Open AccessTumour necrosis factor α mediated apoptosis in murine macrophages by Salmonella enterica serovar Typhi under oxidative stress
Author(s) -
Chanana Vishal,
Majumdar Siddharth,
Rishi Praveen
Publication year - 2006
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2006.00090.x
Subject(s) - biology , oxidative stress , apoptosis , microbiology and biotechnology , tumor necrosis factor alpha , necrosis , salmonella enterica , macrophage , programmed cell death , superoxide dismutase , immunology , innate immune system , immune system , salmonella , in vitro , biochemistry , bacteria , genetics
Invasive Salmonella has been reported to induce apoptosis of macrophages as part of its infection process, which may allow it to avoid detection by the innate immune system. However, the induction of apoptosis under the different host environments remains to be examined, including the oxidative stress experienced by pathogens in the macrophage milieu. To simulate in vivo oxidative conditions, Salmonella enterica serovar Typhi was grown in the presence of hydrogen peroxide and its ability to induce apoptosis of murine macrophages was assessed. Analysis of data revealed that oxidative stressed S . Typhi caused apoptotic cell death in 51% of macrophages, whereas S . Typhi grown under normal conditions accounted for apoptotic cell death in only 32% of macrophages. A significant increase in the levels of oxidants and decrease in the antioxidant was also observed which correlated with the increased generation of tumour necrosis factor α, interleukin‐1α and interleukin‐6. These results suggest that tumour necrosis factor α in conjunction with other cytokines may induce apoptotic cell death through the up‐regulation of lipid peroxidation and down‐regulation of superoxide dismutase. This finding may help us to understand better the host–pathogen interactions and may be of clinical importance in the development of preventive intervention against infection.