Publications by authors named "M Lamkanfi"

Inflammasomes are crucial mediators of both antimicrobial host defense and inflammatory pathology, requiring stringent regulation at multiple levels. This review explores the pivotal role of mitogen-activated protein kinase (MAPK) signaling in modulating inflammasome activation through various regulatory mechanisms. We detail recent advances in understanding MAPK-mediated regulation of NLRP3 inflammasome priming, licensing and activation, with emphasis on MAPK-induced activator protein-1 (AP-1) signaling in NLRP3 priming, ERK1 and JNK in NLRP3 licensing, and TAK1 in connecting death receptor signaling to NLRP3 inflammasome activation.

View Article and Find Full Text PDF
Article Synopsis
  • Neuroinflammation plays a significant role in Alzheimer's disease, with the NLRP3 inflammasome being crucial in this process by promoting the maturation of inflammatory cytokines like IL-1β and IL-18 and influencing tau phosphorylation.
  • This study utilized organotypic brain slice cultures and various mouse models to examine how tau seeds activate the NLRP3 inflammasome and how inhibiting NLRP3 might affect tau pathology.
  • Results indicated that NLRP3 activation is linked to increased tau pathology and neurodegeneration, showcasing its potential as a therapeutic target in Alzheimer's disease treatment.
View Article and Find Full Text PDF

Background & Aims: Liver macrophages fulfill various homeostatic functions and represent an essential line of defense against pathogenic insults. However, it remains unclear whether a history of infectious disease in the liver leads to long-term alterations to the liver macrophage compartment.

Methods: We utilized a curable model of parasitic infection invoked by the protozoan parasite Trypanosoma brucei brucei to investigate whether infection history can durably reshape hepatic macrophage identity and function.

View Article and Find Full Text PDF

Pyroptosis is a lytic cell death mode that helps limit the spread of infections and is also linked to pathology in sterile inflammatory diseases and autoimmune diseases. During pyroptosis, inflammasome activation and the engagement of caspase-1 lead to cell death, along with the maturation and secretion of the inflammatory cytokine interleukin-1β (IL-1β). The dominant effect of IL-1β in promoting tissue inflammation has clouded the potential influence of other factors released from pyroptotic cells.

View Article and Find Full Text PDF