126
Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithe...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Irving, Aaron [verfasserIn] |
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| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
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| Umfang: |
2 |
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| Übergeordnetes Werk: |
Enthalten in: The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types - McLaughlin, Richard J. ELSEVIER, 2022, the official journal of the International Cytokine Society, Oxford [u.a.] |
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| Übergeordnetes Werk: |
volume:63 ; year:2013 ; number:3 ; pages:272-273 ; extent:2 |
| Links: |
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| DOI / URN: |
10.1016/j.cyto.2013.06.129 |
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| 520 | |a Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. | ||
| 520 | |a Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. | ||
| 700 | 1 | |a Turner, Lorinda |4 oth | |
| 700 | 1 | |a Mimuro, Hitomi |4 oth | |
| 700 | 1 | |a Sasakawa, Chihiro |4 oth | |
| 700 | 1 | |a Kufer, Thomas |4 oth | |
| 700 | 1 | |a Philpott, Dana |4 oth | |
| 700 | 1 | |a Ferrero, Richard |4 oth | |
| 700 | 1 | |a Kaparakis-Liaskos, Maria |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a McLaughlin, Richard J. ELSEVIER |t The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |d 2022 |d the official journal of the International Cytokine Society |g Oxford [u.a.] |w (DE-627)ELV008219540 |
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10.1016/j.cyto.2013.06.129 doi GBVA2013017000028.pica (DE-627)ELV022162291 (ELSEVIER)S1043-4666(13)00403-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Irving, Aaron verfasserin aut 126 2013transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Turner, Lorinda oth Mimuro, Hitomi oth Sasakawa, Chihiro oth Kufer, Thomas oth Philpott, Dana oth Ferrero, Richard oth Kaparakis-Liaskos, Maria oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:272-273 extent:2 https://doi.org/10.1016/j.cyto.2013.06.129 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 272-273 2 045F 570 |
| spelling |
10.1016/j.cyto.2013.06.129 doi GBVA2013017000028.pica (DE-627)ELV022162291 (ELSEVIER)S1043-4666(13)00403-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Irving, Aaron verfasserin aut 126 2013transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Turner, Lorinda oth Mimuro, Hitomi oth Sasakawa, Chihiro oth Kufer, Thomas oth Philpott, Dana oth Ferrero, Richard oth Kaparakis-Liaskos, Maria oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:272-273 extent:2 https://doi.org/10.1016/j.cyto.2013.06.129 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 272-273 2 045F 570 |
| allfields_unstemmed |
10.1016/j.cyto.2013.06.129 doi GBVA2013017000028.pica (DE-627)ELV022162291 (ELSEVIER)S1043-4666(13)00403-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Irving, Aaron verfasserin aut 126 2013transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Turner, Lorinda oth Mimuro, Hitomi oth Sasakawa, Chihiro oth Kufer, Thomas oth Philpott, Dana oth Ferrero, Richard oth Kaparakis-Liaskos, Maria oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:272-273 extent:2 https://doi.org/10.1016/j.cyto.2013.06.129 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 272-273 2 045F 570 |
| allfieldsGer |
10.1016/j.cyto.2013.06.129 doi GBVA2013017000028.pica (DE-627)ELV022162291 (ELSEVIER)S1043-4666(13)00403-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Irving, Aaron verfasserin aut 126 2013transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Turner, Lorinda oth Mimuro, Hitomi oth Sasakawa, Chihiro oth Kufer, Thomas oth Philpott, Dana oth Ferrero, Richard oth Kaparakis-Liaskos, Maria oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:272-273 extent:2 https://doi.org/10.1016/j.cyto.2013.06.129 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 272-273 2 045F 570 |
| allfieldsSound |
10.1016/j.cyto.2013.06.129 doi GBVA2013017000028.pica (DE-627)ELV022162291 (ELSEVIER)S1043-4666(13)00403-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl Irving, Aaron verfasserin aut 126 2013transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. Turner, Lorinda oth Mimuro, Hitomi oth Sasakawa, Chihiro oth Kufer, Thomas oth Philpott, Dana oth Ferrero, Richard oth Kaparakis-Liaskos, Maria oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:272-273 extent:2 https://doi.org/10.1016/j.cyto.2013.06.129 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 272-273 2 045F 570 |
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English |
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Enthalten in The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types Oxford [u.a.] volume:63 year:2013 number:3 pages:272-273 extent:2 |
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Enthalten in The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types Oxford [u.a.] volume:63 year:2013 number:3 pages:272-273 extent:2 |
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The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |
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Irving, Aaron @@aut@@ Turner, Lorinda @@oth@@ Mimuro, Hitomi @@oth@@ Sasakawa, Chihiro @@oth@@ Kufer, Thomas @@oth@@ Philpott, Dana @@oth@@ Ferrero, Richard @@oth@@ Kaparakis-Liaskos, Maria @@oth@@ |
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Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. |
| abstractGer |
Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. |
| abstract_unstemmed |
Outer Membrane Vesicles (OMVs) are bi-layered spherical nanostructures shed by all Gram negative bacteria as part of their normal growth process, and throughout the course of infection, both in vitro and in vivo. OMVs deliver peptidoglycan (PG) from Gram negative pathogens into non-phagocytic epithelial cells. Once internalised, the Pattern Recognition Receptor Nucleotide Oligomerization Domain 1 (NOD1) which detects bacterial PG is essential for the development of OMV-dependent immune-responses in vivo. Here, we characterize the mechanisms whereby PG-containing OMVs initiate innate immune responses, via NOD1-dependent autophagy, as evidenced by the formation of autophagic puncta. Additionally we show this NOD1-response is cell type specific, not occurring in macrophages but occurring in various fibroblast and epithelial lines and primary human epithelial cells. In addition, knockdown of NOD1 or NOD1-/- MEFs are deficient in OMV-induced autophagy and loss of critical components in autophagy results in reduced inflammatory responses to OMVs. We show that NOD1 is triggered by direct association to PG, and this recruits the adaptor RIP2. Inhibition of the RIP2 kinase results in a loss of both autophagy and IL-8 production in response to bacterial OMVs. This work highlights an essential role for NOD1 in sensing bacterial PG, delivered intracellularly through OMVs and activating autophagy, which proves critical for the OMV-induced inflammatory response. |
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