Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro

The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Zylfi Memedovski [verfasserIn] Evan Czerwonka [verfasserIn] Jin Han [verfasserIn] Joshua Mayer [verfasserIn] Margaret Luce [verfasserIn] Lucas C. Klemm [verfasserIn] Mary L. Hall [verfasserIn] Alejandro M. S. Mayer [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	microglia lipopolysaccharide neuroinflammation periodontitis

Übergeordnetes Werk:	In: Toxins - MDPI AG, 2010, 12(2020), 5, p 333
Übergeordnetes Werk:	volume:12 ; year:2020 ; number:5, p 333

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/toxins12050333

Katalog-ID:	DOAJ079087361

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allfields	10.3390/toxins12050333 doi (DE-627)DOAJ079087361 (DE-599)DOAJd97de2b511fa4b3b820db0e3b6bb6757 DE-627 ger DE-627 rakwb eng Zylfi Memedovski verfasserin aut Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines. microglia <i<Porphyromonas gingivalis</i< <i<Escherichia coli</i< lipopolysaccharide neuroinflammation periodontitis Medicine R Evan Czerwonka verfasserin aut Jin Han verfasserin aut Joshua Mayer verfasserin aut Margaret Luce verfasserin aut Lucas C. Klemm verfasserin aut Mary L. Hall verfasserin aut Alejandro M. S. Mayer verfasserin aut In Toxins MDPI AG, 2010 12(2020), 5, p 333 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:12 year:2020 number:5, p 333 https://doi.org/10.3390/toxins12050333 kostenfrei https://doaj.org/article/d97de2b511fa4b3b820db0e3b6bb6757 kostenfrei https://www.mdpi.com/2072-6651/12/5/333 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2020 5, p 333
spelling	10.3390/toxins12050333 doi (DE-627)DOAJ079087361 (DE-599)DOAJd97de2b511fa4b3b820db0e3b6bb6757 DE-627 ger DE-627 rakwb eng Zylfi Memedovski verfasserin aut Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines. microglia <i<Porphyromonas gingivalis</i< <i<Escherichia coli</i< lipopolysaccharide neuroinflammation periodontitis Medicine R Evan Czerwonka verfasserin aut Jin Han verfasserin aut Joshua Mayer verfasserin aut Margaret Luce verfasserin aut Lucas C. Klemm verfasserin aut Mary L. Hall verfasserin aut Alejandro M. S. Mayer verfasserin aut In Toxins MDPI AG, 2010 12(2020), 5, p 333 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:12 year:2020 number:5, p 333 https://doi.org/10.3390/toxins12050333 kostenfrei https://doaj.org/article/d97de2b511fa4b3b820db0e3b6bb6757 kostenfrei https://www.mdpi.com/2072-6651/12/5/333 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2020 5, p 333
allfields_unstemmed	10.3390/toxins12050333 doi (DE-627)DOAJ079087361 (DE-599)DOAJd97de2b511fa4b3b820db0e3b6bb6757 DE-627 ger DE-627 rakwb eng Zylfi Memedovski verfasserin aut Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines. microglia <i<Porphyromonas gingivalis</i< <i<Escherichia coli</i< lipopolysaccharide neuroinflammation periodontitis Medicine R Evan Czerwonka verfasserin aut Jin Han verfasserin aut Joshua Mayer verfasserin aut Margaret Luce verfasserin aut Lucas C. Klemm verfasserin aut Mary L. Hall verfasserin aut Alejandro M. S. Mayer verfasserin aut In Toxins MDPI AG, 2010 12(2020), 5, p 333 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:12 year:2020 number:5, p 333 https://doi.org/10.3390/toxins12050333 kostenfrei https://doaj.org/article/d97de2b511fa4b3b820db0e3b6bb6757 kostenfrei https://www.mdpi.com/2072-6651/12/5/333 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2020 5, p 333
allfieldsGer	10.3390/toxins12050333 doi (DE-627)DOAJ079087361 (DE-599)DOAJd97de2b511fa4b3b820db0e3b6bb6757 DE-627 ger DE-627 rakwb eng Zylfi Memedovski verfasserin aut Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines. microglia <i<Porphyromonas gingivalis</i< <i<Escherichia coli</i< lipopolysaccharide neuroinflammation periodontitis Medicine R Evan Czerwonka verfasserin aut Jin Han verfasserin aut Joshua Mayer verfasserin aut Margaret Luce verfasserin aut Lucas C. Klemm verfasserin aut Mary L. Hall verfasserin aut Alejandro M. S. Mayer verfasserin aut In Toxins MDPI AG, 2010 12(2020), 5, p 333 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:12 year:2020 number:5, p 333 https://doi.org/10.3390/toxins12050333 kostenfrei https://doaj.org/article/d97de2b511fa4b3b820db0e3b6bb6757 kostenfrei https://www.mdpi.com/2072-6651/12/5/333 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2020 5, p 333
allfieldsSound	10.3390/toxins12050333 doi (DE-627)DOAJ079087361 (DE-599)DOAJd97de2b511fa4b3b820db0e3b6bb6757 DE-627 ger DE-627 rakwb eng Zylfi Memedovski verfasserin aut Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines. microglia <i<Porphyromonas gingivalis</i< <i<Escherichia coli</i< lipopolysaccharide neuroinflammation periodontitis Medicine R Evan Czerwonka verfasserin aut Jin Han verfasserin aut Joshua Mayer verfasserin aut Margaret Luce verfasserin aut Lucas C. Klemm verfasserin aut Mary L. Hall verfasserin aut Alejandro M. S. Mayer verfasserin aut In Toxins MDPI AG, 2010 12(2020), 5, p 333 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:12 year:2020 number:5, p 333 https://doi.org/10.3390/toxins12050333 kostenfrei https://doaj.org/article/d97de2b511fa4b3b820db0e3b6bb6757 kostenfrei https://www.mdpi.com/2072-6651/12/5/333 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2020 5, p 333
language	English
source	In Toxins 12(2020), 5, p 333 volume:12 year:2020 number:5, p 333
sourceStr	In Toxins 12(2020), 5, p 333 volume:12 year:2020 number:5, p 333
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	microglia <i<Porphyromonas gingivalis</i< <i<Escherichia coli</i< lipopolysaccharide neuroinflammation periodontitis Medicine R
isfreeaccess_bool	true
container_title	Toxins
authorswithroles_txt_mv	Zylfi Memedovski @@aut@@ Evan Czerwonka @@aut@@ Jin Han @@aut@@ Joshua Mayer @@aut@@ Margaret Luce @@aut@@ Lucas C. Klemm @@aut@@ Mary L. Hall @@aut@@ Alejandro M. S. Mayer @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	610604236
id	DOAJ079087361
language_de	englisch
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After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). 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author	Zylfi Memedovski
spellingShingle	Zylfi Memedovski misc microglia misc <i<Porphyromonas gingivalis</i< misc <i<Escherichia coli</i< misc lipopolysaccharide misc neuroinflammation misc periodontitis misc Medicine misc R Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro
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topic_title	Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro microglia <i<Porphyromonas gingivalis</i< <i<Escherichia coli</i< lipopolysaccharide neuroinflammation periodontitis
topic	misc microglia misc <i<Porphyromonas gingivalis</i< misc <i<Escherichia coli</i< misc lipopolysaccharide misc neuroinflammation misc periodontitis misc Medicine misc R
topic_unstemmed	misc microglia misc <i<Porphyromonas gingivalis</i< misc <i<Escherichia coli</i< misc lipopolysaccharide misc neuroinflammation misc periodontitis misc Medicine misc R
topic_browse	misc microglia misc <i<Porphyromonas gingivalis</i< misc <i<Escherichia coli</i< misc lipopolysaccharide misc neuroinflammation misc periodontitis misc Medicine misc R
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title	Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro
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title_full	Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro
author_sort	Zylfi Memedovski
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author_browse	Zylfi Memedovski Evan Czerwonka Jin Han Joshua Mayer Margaret Luce Lucas C. Klemm Mary L. Hall Alejandro M. S. Mayer
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title_sort	classical and alternative activation of rat microglia treated with ultrapure <i<porphyromonas gingivalis</i< lipopolysaccharide in vitro
title_auth	Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro
abstract	The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines.
abstractGer	The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines.
abstract_unstemmed	The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium <i<Porphyromonas gingivalis</i< (<i<P. gingivalis</i<) and the development of neuroinflammation remains under investigation. Recently, <i<P. gingivalis</i< lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure <i<P. gingivalis</i< LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O<sub<2</sub<<sup<−</sup<), thromboxane B<sub<2</sub< (TXB<sub<2</sub<), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines.
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title_short	Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro
url	https://doi.org/10.3390/toxins12050333 https://doaj.org/article/d97de2b511fa4b3b820db0e3b6bb6757 https://www.mdpi.com/2072-6651/12/5/333 https://doaj.org/toc/2072-6651
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After an 18-h exposure of microglia to <i<P. gingivalis</i< LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL <i<P. gingivalis</i< LPS increased O<sub<2</sub<<sup<−</sup< generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL <i<P. gingivalis</i< LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O<sub<2</sub<<sup<−</sup< generation; 100,000 ng/mL <i<P. gingivalis</i< LPS sustained O<sub<2</sub<<sup<−</sup< production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although <i<P. gingivalis</i< LPS was less potent than <i<Escherichia coli</i< (<i<E. coli</i<) LPS in stimulating TXB<sub<2</sub<, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O<sub<2</sub<<sup<−</sup<, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure <i<P. gingivalis</i< LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">microglia</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<Porphyromonas gingivalis</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<Escherichia coli</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">lipopolysaccharide</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">neuroinflammation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">periodontitis</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Medicine</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">R</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Evan Czerwonka</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jin Han</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Joshua Mayer</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Margaret Luce</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Lucas C. 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Classical and Alternative Activation of Rat Microglia Treated with Ultrapure <i<Porphyromonas gingivalis</i< Lipopolysaccharide In Vitro

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