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Overall, CD14/TLR4 signalling seems to be critical for intestinal barrier function and for the crosstalk between B cells and the epithelium, underlining that CD14 serves as a protective modulator of intestinal homeostasis.
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Investigations on the variant of CD14 gene revealed negative association among ischemic stroke patients; however, a significant association was observed for hemorrhagic stroke following dominant and recessive genotypic model.
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this paper shows that CD14 gene silencing alters the microRNA expression profile of RAW264.7 cells stimulated by Brucella melitensis infection
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Data show that multiple phagocytes are capable of hyperactivation in response to oxPAPC, with CD14 antigen acting as the earliest regulator in this process, serving to capture and transport these lipids to promote inflammatory cell fate decisions.
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Data (including data from studies conducted in cells from knockout mice) suggest that signaling via Lpar1, Cd14, and Scara1 mediates uptake of oxidized LDL by macrophages leading to foam cell formation; lysophosphatidic acid (LPA) induces expression of Cd14 and Scara1 in macrophages. (Lpar1 = LPA receptor 1; Cd14 = monocyte differentiation antigen CD14; Scara1 = scavenger receptor class A type I)
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Stimulation of murine peritoneal macrophages with LPS induces biphasic accumulation of PI(4,5)P2 with peaks at 10 and 60-90 min that was abrogated when CD14 was removed from the cell surface.
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these results indicate that CD14 is a co-receptor of TLR4 in the S100A9-induced cytokine response.
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this study shows that lipid rafts may serve as sites in which LPS receptors (CD14) are sorted for endocytosis, rather than being platforms for the assembly of TLR4-centered signaling complexes
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These findings suggested that the degree of lung injury was reduced during the acute inflammatory reaction when NFkappaB was inhibited, and that the expression of sphingomyelin synthase 2 may affect the induction of the NFkappaB pathway by lipopolysaccharide through CD14.
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Results demonstrate remarkable sophistication of microglial CD14 in enabling, facilitating and moderating innate immune responses to infectious and non-infectious CNS threats of diverse kinds
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CD14-mediated lipid signaling induced epithelial apoptosis, whereas TLR4 antagonistically promoted cell survival and cancer development.
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fucosyllactose directly inhibits lipopolysaccharide-mediated inflammation during E. coli infection of intestinal epithelial cells through attenuation of CD14 induction.
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studies revealed a novel physical association between SP-R210S, CD14, and SR-A leading to an enhanced response to LPS, and found that SP-R210L and SP-R210S regulate internalization of CD14 via distinct macropinocytosis-like mechanisms
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Data indicate that Toll-like receptor 4 (TLR4) endocytosis and the TIR-domain-containing adapter-inducing IFN-beta (TRIF)-signaling pathway in macrophages during endotoxin tolerance in the absence of cluster of differentiation 14 (CD14).
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27OHChol can prime monocytes/macrophages by up-regulation of CD14 such that LPS-mediated inflammatory reaction is accelerated, thereby contributing to aggravated development of atherosclerotic lesions.
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microglial HSPGs facilitate CD14-dependent TLR4 activation and that heparanase can modulate this mechanism
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Data show that guanine nucleotide-binding protein G(i) subunit alpha-1 and alpha-3 (Galphai1/3) can interact with CD14 antigen/Grb2-associated binding protein Gab1, which modulates macrophage polarization in vitro and in vivo.
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In acute lung injury, lipopolysaccharide induced alveolar macrophage necrosis via CD14 and the P2X7 receptor leading to interleukin-1alpha release.
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We demonstrated that TLR2, TLR4 and CD14 receptors sense Tityus serrulatus venom (TsV) and its major component, toxin 1 (Ts1), to mediate cytokine and lipid mediator production.
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Gene expression of the anti-inflammatory cytokine IL-13 in prion-infected CD14(-/-) mice was temporarily upregulated at 75dpi, whereas IL-13 gene expression was not upregulated in prion-infected WT mice.
