Inka Sastalla

TL;DR: It is shown that LT cleaves rat Nlrp1 and this cleavage is required for toxin-induced inflammasome activation, IL-1 β release, and macrophage pyroptosis and a new, physiologically relevant protein substrate of LT is identified.

TL;DR: It is found that CGN taken from healthy volunteers but not from patients with AD were associated with enhanced barrier function, innate immunity activation, and control of S. aureus, suggesting that a live-biotherapeutic approach may hold promise for treatment of patients withAD.

TL;DR: An inverse relationship between murine macrophage sensitivity to lethal toxin and mouse susceptibility to spore infection is confirmed, and roles for Nlrp1bS, caspase-1, and IL-1β in countering anthrax infection are established.

TL;DR: The results suggest that the resistance of NOD/LtJ macrophages to LT, and the inability of the Nlrp1b protein expressed in these cells to be activated by the toxin are likely due to polymorphisms other than those at the LF cleavage sites.

TL;DR: It is concluded that activation of the inflammatory programmed cell death pathway in macrophages could constitute an important pathogenic mechanism by which S. pyogenes evades host immune defences and causes disease.