TY - JOUR
T1 - The inhibition of lipopolysaccharide-induced tumor necrosis factor-α and nitric oxide production by Clostridium perfringens α-toxin and its relation to α-toxin-induced intracellular ceramide generation
AU - Tumurkhuu, Gantsetseg
AU - Koide, Naoki
AU - Dagvadorj, Jargalsaikhan
AU - Shadat Mohammod Noman, Abu
AU - Iftekar-E-Khuda, Imtiaz
AU - Naiki, Yoshikazu
AU - Komatsu, Takayuki
AU - Yoshida, Tomoaki
AU - Oda, Masataka
AU - Nagahama, Masahiro
AU - Sakurai, Jun
AU - Yokochi, Takashi
N1 - Funding Information:
This work was supported by in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan. We are grateful to K. Takahashi and A. Morikawa for the technical assistance.
PY - 2009/12
Y1 - 2009/12
N2 - The effect of Clostridium perfringens α-toxin on production of tumor necrosis factor (TNF)-α and nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells was studied. The pretreatment of wild type α-toxin, but not the inactive mutant, significantly decreased LPS-induced TNF-α and NO production. α-Toxin inhibited the expression of TNF-α and an inducible type of NO synthase protein and mRNA. Furthermore, it inhibited the phosphorylation of IκB-α and p65 NF-κB subunit, and the NF-κB luciferase reporter gene activity in LPS-stimulated cells. The pretreatment of α-toxin increased the level of intracellular ceramide. Taken together, Clostridium perfringens α-toxin pretreatment was suggested to inhibit LPS-induced TNF-α and NO production through the inhibition of NF-κB activation. The relationship between α-toxin-induced intracellular ceramide generation and the NF-κB inhibition is discussed.
AB - The effect of Clostridium perfringens α-toxin on production of tumor necrosis factor (TNF)-α and nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells was studied. The pretreatment of wild type α-toxin, but not the inactive mutant, significantly decreased LPS-induced TNF-α and NO production. α-Toxin inhibited the expression of TNF-α and an inducible type of NO synthase protein and mRNA. Furthermore, it inhibited the phosphorylation of IκB-α and p65 NF-κB subunit, and the NF-κB luciferase reporter gene activity in LPS-stimulated cells. The pretreatment of α-toxin increased the level of intracellular ceramide. Taken together, Clostridium perfringens α-toxin pretreatment was suggested to inhibit LPS-induced TNF-α and NO production through the inhibition of NF-κB activation. The relationship between α-toxin-induced intracellular ceramide generation and the NF-κB inhibition is discussed.
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U2 - 10.1016/j.ijmm.2009.04.003
DO - 10.1016/j.ijmm.2009.04.003
M3 - Article
C2 - 19467928
AN - SCOPUS:70350569387
VL - 299
SP - 554
EP - 562
JO - International Journal of Medical Microbiology
JF - International Journal of Medical Microbiology
SN - 1438-4221
IS - 8
ER -