In the present study, we investigated the effect of APO on the activation of inflammasomes from various perspectives, and we observed that APO significantly inhibited activation of the NLRP3 and AIM2 inflammasomes but not the activation of NLRC4
(2) manifestaron que la activacion del inflamasoma NLRC4
requeria de la presencia simultanea de un sistema de secrecion intacto tipo III (T3SS) o tipo IV (T4SS) necesario para el ingreso de los factores de virulencia bacterianos y de pequenas cantidades de flagelina; en particular se ha demostrado que es una region en el extremo C-terminal de flagelina la que activa el inflamasoma a traves del receptor NLRC4
Izrael-Tomasevic et al., "Phosphorylation of NLRC4
is critical for inflammasome activation," Nature, vol.
inflammasome-mediated production of IL-1beta modulates mucosal immunity in the lung against gram-negative bacterial infection," Journal of Immunology, vol.
Yudkovsky et al., "Innate immune detection of the type III secretion apparatus through the NLRC4
inflammasome," Proceedings of the National Academy of Sciences of the United States of America, vol.
Lenart et al., "AIM2 and NLRC4
inflammasomes contribute with ASC to acute brain injury independently of NLRP3," Proceedings of the National Academy of Sciences, vol.
NLR proteins NLRP3, NLRP1, and NLRC4
as well as a recently identified HIN-200 protein absent in melanoma 2 (AIM2) are activated by pathogen- and danger-associated molecular patterns (PAMPs and DAMPs, resp.) results in the recruitment of the inflammasome-adaptor protein, ASC (also known as PYCARD), and procaspase-1 .
To further illuminate the noncanonical inflammasome signaling pathway in IPEC-J2 cells, we additionally included the following genes in our analyses: inflammasome-forming NLRC4
(NLR family, CARD domain containing 4), the adapter ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1, and toll-like receptor (TLR) 4 (Supplementary Tables 6 and 7).
Another NLR protein, NLR family CARD domain-containing protein 4 (NLRC4
), has been observed in heart diseases, and this study showed that NLRC4
inflammasome was hyperactivated by mitochondrial DNA in cardiomyocytes in a type 2 diabetes mouse model after MI .
The best known activator of CASP1 is the inflammasome, a complex of proteins (such as nucleotide-binding domain leucine-rich repeat containing proteins NLRP1 and NPLR3, NLR family CARD domain-containing protein NLRC4
, and the apoptosis-associated speck-like protein containing a CASP recruitment domain or in short ASC) that are aggregated by various inflammatory conditions in immune and glial cells and lead to the CASP1 cleavage .