Enhancement of the anti-Salmonella immune response in CD154-deficient mice by an attenuated, IFN-γ-expressing, strain of Salmonella enterica serovar Typhimurium

2012 ◽  
Vol 52 (6) ◽  
pp. 326-335 ◽  
Author(s):  
Samia M. Al-Ojali ◽  
C.B. Tara Moore ◽  
Maria J. Fernandez-Cabezudo ◽  
Basel K. al-Ramadi
Keyword(s):  
Immune Response ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Serovar Typhimurium ◽  
Ifn Γ ◽  
Deficient Mice

scholarly journals Caspase-1-Mediated Activation of Interleukin-1β (IL-1β) and IL-18 Contributes to Innate Immune Defenses against Salmonella enterica Serovar Typhimurium Infection

2006 ◽  
Vol 74 (8) ◽  
pp. 4922-4926 ◽  
Author(s):  
Bärbel Raupach ◽  
Soo-Kyung Peuschel ◽  
Denise M. Monack ◽  
Arturo Zychlinsky
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Systemic Infection ◽  
Immune Defense ◽  
Innate Immune ◽  
Interleukin 1Β ◽  
Intestinal Phase ◽  
Caspase 1 ◽  
Serovar Typhimurium ◽  
Deficient Mice

ABSTRACTCaspase-1 (Casp-1) mediates the processing of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18 to their mature forms. Casp-1-deficient mice succumb more rapidly toSalmonellachallenge than do wild-type animals. Both Casp-1 substrates, IL-18 and IL-1β, are relevant for control ofSalmonella entericaserovar Typhimurium. We used IL-18−/−and IL-1β−/−mice in addition to administration of recombinant IL-18 to Casp-1−/−mice to demonstrate that IL-18 is important for resistance to the systemic infection but not for resistance to the intestinal phase of the infection. This suggests that IL-1β is critical for the intestinal phase of the disease. Thus, we show that Casp-1 is essential for host innate immune defense againstS. entericaserovar Typhimurium and that Casp-1 substrates are required at distinct times and anatomical sites.

scholarly journals c-Fos-Deficient Mice Are Susceptible to Salmonella enterica Serovar Typhimurium Infection

2006 ◽  
Vol 75 (3) ◽  
pp. 1520-1523 ◽  
Author(s):  
Kenta Maruyama ◽  
Gen-ichiro Sano ◽  
Neelanjan Ray ◽  
Yasunari Takada ◽  
Koichi Matsuo
Keyword(s):  
Cell Death ◽  
Transcription Factor ◽  
Proinflammatory Cytokines ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Enhanced Production ◽  
Serovar Typhimurium ◽  
Deficient Mice

ABSTRACT c-Fos is a component of transcription factor AP-1. We show that macrophages lacking c-Fos exhibit enhanced production of proinflammatory cytokines, potentiated NF-κB phosphorylation, and increased cell death following Salmonella enterica serovar Typhimurium infection. Furthermore, mice lacking c-Fos are highly susceptible to infection, suggesting that c-Fos confers resistance to Salmonella infection in mice.

Sign in / Sign up

Export Citation Format

Share Document