Fig. 1: Pro-inflammatory response of TLR4, MyD88 or TLR2 knockout macrophages to Abeta42(Aβ) oligomers and fibrils. | Communications Biology

Fig. 1: Pro-inflammatory response of TLR4, MyD88 or TLR2 knockout macrophages to Abeta42(Aβ) oligomers and fibrils.

From: Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death

Fig. 1

Cells (WT: wild type, MyD88−/−: MyD88 knockout, TLR4−/−: TLR4 knock out and TLR2−/−: TLR2 knockout) were stimulated with Aβ Fibrils (0.1–400 nM) and Aβ oligomers together with monomer (total monomer concentration 0.02–80 μM) for 24 h. The levels of the pro-inflammatory mediators TNF-α and IL-1β were measured. a TNF-α production remained unchanged at all concentrations with the addition of Fibrils (n = 5, ±sem). b TNF-α production significantly increases with increasing oligomer concentrations in all except the TLR4 knockout cells (n = 5, ±sem). c IL-1β levels production significantly increases with increasing oligomer concentrations in all except the TLR4 knockout cells (n = 5, mean ± sem).

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