Patricia L. Fernández

TL;DR: It is demonstrated that heme, but not its analogs/precursors, induced tumor necrosis factor-α (TNF-α) secretion by macrophages dependently on MyD88, TLR4, and CD14, and these findings support the concept that the broad ligand specificity ofTLR4 and the different activation profiles might in part reside in its ability to recognize different ligands in different binding sites.

TL;DR: It is shown that heme induces IL-1β processing through the activation of the nucleotide-binding domain and leucine rich repeat containing family, pyrin domain containing 3 (NLRP3) inflammasome in macrophages, suggesting that among NLRP3 activators, heme has common as well as unique requirements to trigger inflammaome activation.

TL;DR: The role of several receptors expressed on microglia in Aβ recognition, uptake, and signaling, and their implications for AD pathogenesis are discussed.

TL;DR: It is shown that heme caused early macrophage death characterized by the loss of plasma membrane integrity and morphologic features resembling necrosis, and 2 synergistic mechanisms were revealed: TLR4/Myd88-dependent expression of TNF andTLR4-independent generation of ROS.

TL;DR: The results indicate that heme activates neutrophils through signaling pathways that are characteristic of chemoattractant molecules and suggest that mesoporphyrins might prove valuable in the treatment of the inflammatory consequences of hemorrhagic and hemolytic disorders.