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Alteration of Lysosome Fusion and Low-grade Inflammation Mediated by Super-low-dose Endotoxin

Baker, Bianca, Geng, Shuo, Chen, Keqiang, Diao, Na, Yuan, Ruoxi, Xu, Xiguang, Dougherty, Sean, Stephenson, Caroline, Xiong, Huabao, Chu, Hong Wei, Li, Liwu·2015·Journal of Biological Chemistry
DOI 10.1074/jbc.m114.611442
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FIGURE 1 Super-low-dose LPS suppresses lysosome fusion. A , WT macrophages treated with either PBS or LPS (50 pg/ml or 100 ng/ml) were subjected to endosome acidification assays by incorporating pH-sensitive dextran double-labeled with FITC and tetramethylrhodamine. Flow cytometry analyses were performed to monitor the increase in fluorescence intensity, which indicates a decrease in endosomal pH. *, p < 0.05 compared with untreated controls. B , WT macrophages treated with either PBS or 50 pg/ml LPS were subjected to endosome-lysosome fusion assays by sequential incorporation of Alexa Fluor 546-labeled dextran and FITC-labeled zymosan BioParticles. Fluorescence images were obtained with the Zeiss LSM 510 laser-scanning confocal microscope to observe isolated lysosomes ( red ), endosomes ( green ), and fused endolysosomes ( orange ). The percentage of cells with fused endolysosomes is represented in the graph. *, p < 0.05 compared with untreated controls. C , WT macrophages treated with PBS or 50 pg/ml LPS for 2 h were subjected to analyses by transmission electron microscopy. Dark electron-dense lysosome structures can be seen in the samples challenged with 50 pg/ml LPS. D , WT macrophages were treated with either 50 pg/ml or 100 ng/ml LPS for the indicated times. The levels of p62 and GAPDH controls were determined by Western blot analyses. Data represent three experiments. *, p < 0.05 compared with untreated controls. E , WT macrophages were treated with either 50 pg/ml or 100 ng/ml LPS for the indicated times. The levels of phosphorylated ( p ) and total JNK, ERK, and p38 were determined by Western blotting. Data represent three experiments.
FIGURE 1 Super-low-dose LPS suppresses lysosome fusion. A , WT macrophages treated with either PBS or LPS (50 pg/ml or 100 ng/ml) were subjected to endosome acidification assays by incorporating pH-sensitive dextran double-labeled with FITC and tetramethylrhodamine. Flow cytometry analyses were performed to monitor the increase in fluorescence intensity, which indicates a decrease in endosomal pH. *, p < 0.05 compared with untreated controls. B , WT macrophages treated with either PBS or 50 pg/ml LPS were subjected to endosome-lysosome fusion assays by sequential incorporation of Alexa Fluor 546-labeled dextran and FITC-labeled zymosan BioParticles. Fluorescence images were obtained with the Zeiss LSM 510 laser-scanning confocal microscope to observe isolated lysosomes ( red ), endosomes ( green ), and fused endolysosomes ( orange ). The percentage of cells with fused endolysosomes is represented in the graph. *, p < 0.05 compared with untreated controls. C , WT macrophages treated with PBS or 50 pg/ml LPS for 2 h were subjected to analyses by transmission electron microscopy. Dark electron-dense lysosome structures can be seen in the samples challenged with 50 pg/ml LPS. D , WT macrophages were treated with either 50 pg/ml or 100 ng/ml LPS for the indicated times. The levels of p62 and GAPDH controls were determined by Western blot analyses. Data represent three experiments. *, p < 0.05 compared with untreated controls. E , WT macrophages were treated with either 50 pg/ml or 100 ng/ml LPS for the indicated times. The levels of phosphorylated ( p ) and total JNK, ERK, and p38 were determined by Western blotting. Data represent three experiments.CC-BY · From the PDF
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FIGURE 3 Super-low-dose LPS suppresses AMPK and VPS34. WTand Tollip-deficient macrophages were treated with 50 pg/ml LPS for the indicated times. The levels of phosphorylated ( p ) and total AMPK ( A ) and VPS34 ( B ) were determined by Western blot analyses. The relative levels of phosphorylated AMPK and VPS34 were quantified from three experiments. *, p < 0.05 compared with untreated controls.
FIGURE 3 Super-low-dose LPS suppresses AMPK and VPS34. WTand Tollip-deficient macrophages were treated with 50 pg/ml LPS for the indicated times. The levels of phosphorylated ( p ) and total AMPK ( A ) and VPS34 ( B ) were determined by Western blot analyses. The relative levels of phosphorylated AMPK and VPS34 were quantified from three experiments. *, p < 0.05 compared with untreated controls.CC-BY · From the PDF
FIGURE 4 Clearance and removal of Tollip from late endosomes/lysosomesbysuper-low-doseLPS. A , WT macrophagesweretreatedwithPBSor 50 pg/ml LPS for 1 h. Total cell lysates were harvested, and equal amounts of protein lysates were resolved by SDS-PAGE. The levels of Tollip and control GAPDH were visualized by Western blotting. WT macrophages were treated with 50 pg/ml LPS for either 1 h ( B ) or 24 h ( C ). Cells were stained with goat anti-mouse Tollip antibody, followed by Alexa Fluor 488-labeled rabbit antigoat IgG together with either Cy3-conjugated LAMP1-specific antibody ( B ) or MitoTracker Red ( C ). The intracellular distribution of Tollip in late endosomes/ lysosomes or mitochondrial compartments was visualized by confocal fluorescence microscopy.
FIGURE 4 Clearance and removal of Tollip from late endosomes/lysosomesbysuper-low-doseLPS. A , WT macrophagesweretreatedwithPBSor 50 pg/ml LPS for 1 h. Total cell lysates were harvested, and equal amounts of protein lysates were resolved by SDS-PAGE. The levels of Tollip and control GAPDH were visualized by Western blotting. WT macrophages were treated with 50 pg/ml LPS for either 1 h ( B ) or 24 h ( C ). Cells were stained with goat anti-mouse Tollip antibody, followed by Alexa Fluor 488-labeled rabbit antigoat IgG together with either Cy3-conjugated LAMP1-specific antibody ( B ) or MitoTracker Red ( C ). The intracellular distribution of Tollip in late endosomes/ lysosomes or mitochondrial compartments was visualized by confocal fluorescence microscopy.CC-BY · From the PDF
FIGURE 5 Cells with mutant Tollip constitutively localized at late endosomes/lysosomes exhibit lysosome fusion in the presence of super-low-dose LPS. WT and Tollip M240A/F241A mutant MEF cells were treated with PBS or 50 pg/ml LPS for 24 h. A and B , the intracellular distribution of Tollip in late endosomes/lysosomes or mitochondrial compartments was visualized by confocal fluorescence microscopy. Cells were stained with goat anti-mouse Tollip antibody, followed by Alexa Fluor 488-labeled rabbit anti-goat IgG together with either Cy3-conjugated LAMP1-specific antibody ( A ) or MitoTracker Red ( B ). C , fusion of lysosomes with autophagosomes was visualized by staining autophagosomes with Alexa Fluor 488-labeled LC3 ( LCIII ) antibody and Cy3-conjugated LAMP1-specific antibody.
FIGURE 5 Cells with mutant Tollip constitutively localized at late endosomes/lysosomes exhibit lysosome fusion in the presence of super-low-dose LPS. WT and Tollip M240A/F241A mutant MEF cells were treated with PBS or 50 pg/ml LPS for 24 h. A and B , the intracellular distribution of Tollip in late endosomes/lysosomes or mitochondrial compartments was visualized by confocal fluorescence microscopy. Cells were stained with goat anti-mouse Tollip antibody, followed by Alexa Fluor 488-labeled rabbit anti-goat IgG together with either Cy3-conjugated LAMP1-specific antibody ( A ) or MitoTracker Red ( B ). C , fusion of lysosomes with autophagosomes was visualized by staining autophagosomes with Alexa Fluor 488-labeled LC3 ( LCIII ) antibody and Cy3-conjugated LAMP1-specific antibody.CC-BY · From the PDF
FIGURE6 ImpairedwoundrepairandincreasedinflammatorymonocytesinwoundtissuesinTollip-deficientmice. A , WT andTollip-deficient mice were injected intraperitoneally with either PBS or 100 pg/mouse LPS every 3 days for 10 days. On day 10, the lower backs of the mice were punctured with 4-mm full skin-depth wounds and monitored daily for wound size. The ratios of the unhealed wound sizes to the original wounds are plotted ( n > 7). *, p < 0.05; ***, p < 0.001. B , total protein lysates were harvested from wound tissues from WT and Tollip-deficient mice. The levels of phospho-JNK ( p-JNK ), p62, and Tollip were determined by Western blotting. Representative blots are shown. The relative intensities of p62 and phospho-JNK (12 WT samples and six Tollip-deficient samples) were adjusted with GAPDH loading controls and are plotted. *, p < 0.05; ***, p < 0.001.
FIGURE6 ImpairedwoundrepairandincreasedinflammatorymonocytesinwoundtissuesinTollip-deficientmice. A , WT andTollip-deficient mice were injected intraperitoneally with either PBS or 100 pg/mouse LPS every 3 days for 10 days. On day 10, the lower backs of the mice were punctured with 4-mm full skin-depth wounds and monitored daily for wound size. The ratios of the unhealed wound sizes to the original wounds are plotted ( n > 7). *, p < 0.05; ***, p < 0.001. B , total protein lysates were harvested from wound tissues from WT and Tollip-deficient mice. The levels of phospho-JNK ( p-JNK ), p62, and Tollip were determined by Western blotting. Representative blots are shown. The relative intensities of p62 and phospho-JNK (12 WT samples and six Tollip-deficient samples) were adjusted with GAPDH loading controls and are plotted. *, p < 0.05; ***, p < 0.001.CC-BY · From the PDF
FIGURE7 SchematicdiagramoftheroleandregulationofTollipininnate macrophages challenged with super-low-dose endotoxin.
FIGURE7 SchematicdiagramoftheroleandregulationofTollipininnate macrophages challenged with super-low-dose endotoxin.CC-BY · From the PDF

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Metadata

Authors
Baker, B., Geng, S., Chen, K., Diao, N., Yuan, R., Xu, X., Dougherty, S., Stephenson, C., Xiong, H., Chu, H. W., & Li, L.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2015-03
Volume
290
Issue
10
Pages
6670-6678
ISSN
0021-9258
DOI
10.1074/jbc.m114.611442
Cited by
47
References
2
Language
en
Licence
Funders
National Institutes of Health (R01HL115835, AI106287)

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