Diverging pathways for lipopolysaccharide and CD14 in human monocytes

Antal‐Szalmás, Péter; Poppelier, Miriam J.J.G.; Broekhuizen, Roel; Verhoef, J.; Strijp, Jos A. G. van; Kessel, Kok P. M. van

doi:10.1002/1097-0320(20001201)41:4<279::aid-cyto6>3.3.co;2-2

Cited by 6 publications

(6 citation statements)

References 11 publications

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“…The rapid LPS-induced clustering of CD14 in the plasma membrane of J774 cells was accompanied by an overall increase of its content, followed by loss of CD14 from the plasma membrane. Although internalization of CD14-LPS is widely accepted (Zanoni et al, 2011), few reports to date indicate a rapid recruitment of a cytoplasmic pool of CD14 to the plasma membrane shortly after exposure of cells to LPS (Antal-Szalmas et al, 2000;Vasselon et al, 1999). The fairly high increase of CD14 in the plasma membrane of J774 cells found in our electron microscopy studies suggests that the dorsal surface of cells examined in these studies is the preferred site of CD14 recruitment.…”

Section: Discussionmentioning

confidence: 46%

LPS-induced clustering of CD14 triggers generation of PI(4,5)P2

Płóciennikowska

Zdioruk

Traczyk

et al. 2015

Journal of Cell Science

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Bacterial lipopolysaccharide (LPS) induces strong pro-inflammatory reactions after sequential binding to CD14 protein and TLR4 receptor. Here, we show that CD14 controls generation of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P 2 ] in response to LPS binding. In J774 cells and HEK293 cells expressing CD14 exposed to 10-100 ng/ml LPS, the level of PI(4,5)P 2 rose in a biphasic manner with peaks at 5-10 min and 60 min. After 5-10 min of LPS stimulation, CD14 underwent prominent clustering in the plasma membrane, accompanied by accumulation of PI(4,5)P 2 and type-I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) isoforms Iα and Iγ (encoded by Pip5k1a and Pip5k1c, respectively) in the CD14 region. Clustering of CD14 with antibodies, without LPS and TLR4 participation, was sufficient to trigger PI(4,5)P 2 elevation. The newly generated PI(4,5)P 2 accumulated in rafts, which also accommodated CD14 and a large portion of PIP5K Iα and PIP5K Iγ. Silencing of PIP5K Iα and PIP5K Iγ, or application of drugs interfering with PI(4,5)P 2 synthesis and availability, abolished the LPS-induced PI(4,5)P 2 elevation and inhibited downstream pro-inflammatory reactions. Taken together, these data indicate that LPS induces clustering of CD14, which triggers PI(4,5)P 2 generation in rafts that is required for maximal pro-inflammatory signaling of TLR4.

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Section: Discussionmentioning

confidence: 46%

LPS-induced clustering of CD14 triggers generation of PI(4,5)P2

Płóciennikowska

Zdioruk

Traczyk

et al. 2015

Journal of Cell Science

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“…Monocytes have been reported to internalize E. coli using a CD14-dependent pathway (7). In contrast, studies suggest that mCD14 and LPS molecules are internalized independently after association on the cell surface (39). To determine whether phagocytosis was the mechanism responsible for the decreased expression of mCD14, AM were incubated with Bodipy-labeled E. coli at 0, 5, 15, 30, 60, 120, and 240 minutes and bacterial phagocytosis was measured with flow cytometry.…”

Section: Discussionmentioning

confidence: 99%

Differential Regulation of Membrane CD14 Expression and Endotoxin-Tolerance in Alveolar Macrophages

Lin

Frevert

Kajikawa

et al. 2004

Am J Respir Cell Mol Biol

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in part by NIH grants GM37696, HL30542. SUMMARYCD14 is important in the clearance of bacterial pathogens from lungs. However, the mechanisms that regulate the expression of membrane CD14 (mCD14) on alveolar macrophages (AM) have not been studied in detail. This study examines the regulation of mCD14 on AM exposed to Escherichia coli in vivo and in vitro and explores the consequences of changes in mCD14 expression. The expression of mCD14 was decreased on AM exposed to E. coli in vivo and AM incubated with lipopolysaccharide (LPS) or E. coli in vitro. Polymyxin B abolished LPS effects but only partially blocked the effects of E. coli. Blockade of extracellular signal-regulated kinase pathways attenuated LPS and E. coli-induced decrease in mCD14 expression. Inhibition of proteases abrogated the LPS-induced decrease in mCD14 expression on AM and the release of sCD14 into the supernatants, but did not affect the response to E. coli. The production of TNF-α in response to a second challenge with Staphylococcus aureus or zymosan was decreased in AM following incubation with E. coli but not LPS. These studies show that distinct mechanisms regulate the expression of mCD14 and the induction of endotoxin-tolerance in AM and suggest that AM function is impaired at sites of bacterial infection.

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“…Surface-adherent FITC fluorescence on PMN was quenched by the addition of 20 μl of 0·4 % trypan blue solution to each tube before flow cytometry analysis as previously described (Hed et al 1987). The use of trypan blue solution has an effect in fluorescence quenching on attached particles but not ingested particles (Antal-Szalmás et al 2000). Phagocytosis was measured by FACS Calibur (Becton Dickinson Immunocytometry Systems, San Jose, CA, USA) flow cytometry using CELLQuest software.…”

Section: Methodsmentioning

confidence: 99%

Trans-10,cis-12-conjugated linoleic acid increases phagocytosis of porcine peripheral blood polymorphonuclear cellsin vitro

et al. 2007

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Trans-10, cis-12-conjugated linoleic acid (t10c12-CLA) has been shown to alter immune function. PPARg has been shown to potentially play an important role in regulating inflammatory and immune responses by modulating the activity of monocytes and macrophages. Previous studies have indicated that the phagocytic capacity of porcine peripheral blood polymorphonuclear cells (PMN) was enhanced by the culture supernatant fraction from t10c12-CLA-stimulated porcine peripheral blood mononuclear cells (PBMC) but not by t10c12-CLA itself. In the present study, we examined the effects of t10c12-CLA on PPARg and TNF-a expression of porcine PBMC and the phagocytic capacity of PMN. t10c12-CLA increased TNF-a mRNA expression and production by PBMC. The phagocytic capacity of porcine PMN was enhanced by either culture supernatant fraction from PBMC treated with t10c12-CLA or recombinant porcine (rp) TNF-a. Anti-rpTNF-a polyclonal antibody inhibited the enhancement of PMN phagocytic capacity. t10c12-CLA also up regulated PPARg mRNA expression in porcine PBMC. Bisphenol A diglycidyl ether, a PPARg antagonist, not only completely negated the t10c12-CLA-stimulating effects on TNF-a expression and production by porcine PBMC, but also decreased the enhancement of PMN phagocytic capacity by the t10c12-CLA-stimulated porcine PBMC culture supernatant fraction. These results suggest that t10c12-CLA has an immunostimulating effect on porcine PMN phagocytic capacity, which is mediated by TNF-a from PBMC via a PPARg-dependent pathway.

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Diverging pathways for lipopolysaccharide and CD14 in human monocytes

Cited by 6 publications

References 11 publications

LPS-induced clustering of CD14 triggers generation of PI(4,5)P2

LPS-induced clustering of CD14 triggers generation of PI(4,5)P2

Differential Regulation of Membrane CD14 Expression and Endotoxin-Tolerance in Alveolar Macrophages

Trans-10,cis-12-conjugated linoleic acid increases phagocytosis of porcine peripheral blood polymorphonuclear cellsin vitro

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