Title |
Sulforaphane kills Mycobacterium tuberculosis H37Ra and Mycobacterium smegmatis mc2155 through a reactive oxygen species dependent mechanism |
Author |
Yongjie Zhao, Shengwen Shang, Ya Song, Tianyue Li, Mingliang Han, Yuexuan Qin, Meili Wei, Jun Xi*, and Bikui Tang* |
Address |
School of Life Science, Anhui Province Key Laboratory of Immunology in Chronic Diseases, Anhui Key Laboratory of Infection and Immunity, Bengbu Medical College, Bengbu, Anhui 233030, P. R. China |
Bibliography |
Journal of Microbiology, 60(11),1095-1105, 2022,
|
DOI |
10.1007/s12275-022-2284-8
|
Key Words |
Mycobacterium tuberculosis, sulforaphane, redox,
ROS, macrophages |
Abstract |
Mycobacterium tuberculosis (M. tuberculosis) is a highly pathogenic
intracellular pathogen that causes tuberculosis (TB),
the leading cause of mortality from single infections. Redox
homeostasis plays a very important role in the resistance of
M. tuberculosis to antibiotic damage and various environmental
stresses. The antioxidant sulforaphane (SFN) has been
reported to exhibit anticancer activity and inhibit the growth
of a variety of bacteria and fungi. Nonetheless, it remains unclear
whether SFN exhibits anti-mycobacterial activity. Our
results showed that the SFN against M. tuberculosis H37Ra
exhibited bactericidal activity in a time and dose-dependent
manner. The anti-tubercular activity of SFN was significantly
correlated with bacterial reactive oxygen species (ROS) levels.
In addition, SFN promoted the bactericidal effect of macrophages
on intracellular bacteria in a dose-dependent manner,
mediated by increasing intracellular mitochondrial ROS
levels and decreasing cytoplasmic ROS levels. Taken together,
our data revealed the previously unrecognized antimicrobial
functions of SFN. Future studies focusing on the mechanism
of SFN in macrophages against M. tuberculosis are
essential for developing new host-directed therapeutic approaches
against TB. |