Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein
The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gmiterek, Anna [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Schlagwörter: |
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| Umfang: |
13 |
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| Übergeordnetes Werk: |
Enthalten in: Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center - Clark, Leon G. ELSEVIER, 2016, experimental and clinical, München |
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| Übergeordnetes Werk: |
volume:221 ; year:2016 ; number:12 ; pages:1382-1394 ; extent:13 |
| Links: |
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| DOI / URN: |
10.1016/j.imbio.2016.07.007 |
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ELV02427657X |
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| 245 | 1 | 0 | |a Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein |
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| 520 | |a The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. | ||
| 520 | |a The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. | ||
| 650 | 7 | |a Porphyromonas gingivalis |2 Elsevier | |
| 650 | 7 | |a Periodontitis |2 Elsevier | |
| 650 | 7 | |a Cytokine |2 Elsevier | |
| 650 | 7 | |a HmuY |2 Elsevier | |
| 650 | 7 | |a Toll-like receptor |2 Elsevier | |
| 650 | 7 | |a Macrophage |2 Elsevier | |
| 700 | 1 | |a Kłopot, Anna |4 oth | |
| 700 | 1 | |a Wójtowicz, Halina |4 oth | |
| 700 | 1 | |a Trindade, Soraya C. |4 oth | |
| 700 | 1 | |a Olczak, Mariusz |4 oth | |
| 700 | 1 | |a Olczak, Teresa |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Clark, Leon G. ELSEVIER |t Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center |d 2016 |d experimental and clinical |g München |w (DE-627)ELV013869728 |
| 773 | 1 | 8 | |g volume:221 |g year:2016 |g number:12 |g pages:1382-1394 |g extent:13 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.imbio.2016.07.007 |3 Volltext |
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10.1016/j.imbio.2016.07.007 doi GBVA2016006000019.pica (DE-627)ELV02427657X (ELSEVIER)S0171-2985(16)30326-6 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Gmiterek, Anna verfasserin aut Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein 2016transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. Porphyromonas gingivalis Elsevier Periodontitis Elsevier Cytokine Elsevier HmuY Elsevier Toll-like receptor Elsevier Macrophage Elsevier Kłopot, Anna oth Wójtowicz, Halina oth Trindade, Soraya C. oth Olczak, Mariusz oth Olczak, Teresa oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:221 year:2016 number:12 pages:1382-1394 extent:13 https://doi.org/10.1016/j.imbio.2016.07.007 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 221 2016 12 1382-1394 13 045F 570 |
| spelling |
10.1016/j.imbio.2016.07.007 doi GBVA2016006000019.pica (DE-627)ELV02427657X (ELSEVIER)S0171-2985(16)30326-6 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Gmiterek, Anna verfasserin aut Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein 2016transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. Porphyromonas gingivalis Elsevier Periodontitis Elsevier Cytokine Elsevier HmuY Elsevier Toll-like receptor Elsevier Macrophage Elsevier Kłopot, Anna oth Wójtowicz, Halina oth Trindade, Soraya C. oth Olczak, Mariusz oth Olczak, Teresa oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:221 year:2016 number:12 pages:1382-1394 extent:13 https://doi.org/10.1016/j.imbio.2016.07.007 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 221 2016 12 1382-1394 13 045F 570 |
| allfields_unstemmed |
10.1016/j.imbio.2016.07.007 doi GBVA2016006000019.pica (DE-627)ELV02427657X (ELSEVIER)S0171-2985(16)30326-6 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Gmiterek, Anna verfasserin aut Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein 2016transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. Porphyromonas gingivalis Elsevier Periodontitis Elsevier Cytokine Elsevier HmuY Elsevier Toll-like receptor Elsevier Macrophage Elsevier Kłopot, Anna oth Wójtowicz, Halina oth Trindade, Soraya C. oth Olczak, Mariusz oth Olczak, Teresa oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:221 year:2016 number:12 pages:1382-1394 extent:13 https://doi.org/10.1016/j.imbio.2016.07.007 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 221 2016 12 1382-1394 13 045F 570 |
| allfieldsGer |
10.1016/j.imbio.2016.07.007 doi GBVA2016006000019.pica (DE-627)ELV02427657X (ELSEVIER)S0171-2985(16)30326-6 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Gmiterek, Anna verfasserin aut Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein 2016transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. Porphyromonas gingivalis Elsevier Periodontitis Elsevier Cytokine Elsevier HmuY Elsevier Toll-like receptor Elsevier Macrophage Elsevier Kłopot, Anna oth Wójtowicz, Halina oth Trindade, Soraya C. oth Olczak, Mariusz oth Olczak, Teresa oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:221 year:2016 number:12 pages:1382-1394 extent:13 https://doi.org/10.1016/j.imbio.2016.07.007 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 221 2016 12 1382-1394 13 045F 570 |
| allfieldsSound |
10.1016/j.imbio.2016.07.007 doi GBVA2016006000019.pica (DE-627)ELV02427657X (ELSEVIER)S0171-2985(16)30326-6 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Gmiterek, Anna verfasserin aut Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein 2016transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. Porphyromonas gingivalis Elsevier Periodontitis Elsevier Cytokine Elsevier HmuY Elsevier Toll-like receptor Elsevier Macrophage Elsevier Kłopot, Anna oth Wójtowicz, Halina oth Trindade, Soraya C. oth Olczak, Mariusz oth Olczak, Teresa oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:221 year:2016 number:12 pages:1382-1394 extent:13 https://doi.org/10.1016/j.imbio.2016.07.007 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 221 2016 12 1382-1394 13 045F 570 |
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English |
| source |
Enthalten in Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center München volume:221 year:2016 number:12 pages:1382-1394 extent:13 |
| sourceStr |
Enthalten in Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center München volume:221 year:2016 number:12 pages:1382-1394 extent:13 |
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Article |
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Umweltchemie Umwelttoxikologie Medizinische Ökologie |
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immune response of macrophages induced by porphyromonas gingivalis requires hmuy protein |
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Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein |
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The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. |
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The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. |
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The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages. |
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We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Porphyromonas gingivalis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Periodontitis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cytokine</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HmuY</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Toll-like receptor</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Macrophage</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kłopot, Anna</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wójtowicz, Halina</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Trindade, Soraya C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Olczak, Mariusz</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Olczak, Teresa</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Clark, Leon G. ELSEVIER</subfield><subfield code="t">Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center</subfield><subfield code="d">2016</subfield><subfield code="d">experimental and clinical</subfield><subfield code="g">München</subfield><subfield code="w">(DE-627)ELV013869728</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:221</subfield><subfield code="g">year:2016</subfield><subfield code="g">number:12</subfield><subfield code="g">pages:1382-1394</subfield><subfield code="g">extent:13</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.imbio.2016.07.007</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.12</subfield><subfield code="j">Umweltchemie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.13</subfield><subfield code="j">Umwelttoxikologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.13</subfield><subfield code="j">Medizinische Ökologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">221</subfield><subfield code="j">2016</subfield><subfield code="e">12</subfield><subfield code="h">1382-1394</subfield><subfield code="g">13</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
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