Key result
Flotillin deficiency in macrophages strongly inhibited TRIF-dependent endosomal signaling of LPS-activated TLR4 by down-regulating CD14 mRNA and protein levels.
Why the study?
Given the role of membrane rafts, endocytosis, and trafficking in CD14 and TLR4 activity, it was hypothesized that LPS-induced pro-inflammatory macrophage reactions could be modulated by flotillins.
Flotillins modulate macrophage pro-inflammatory responses to LPS by regulating CD14 abundance and trafficking.
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Hypothesis-generating for flotillin targeting in LPS-driven inflammation; leaves open translation to human disease.
Matveichuk et al. (2023) studied this question. Flotillin-2 knockdown (shRNA) vs. Control shRNA was evaluated on TRIF-dependent endosomal signaling of LPS-activated TLR4 (IRF3 phosphorylation) and CD14 abundance. Flotillin deficiency in macrophages strongly inhibited TRIF-dependent endosomal signaling of LPS-activated TLR4 by down-regulating CD14 mRNA and protein levels.
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