The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages
Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many wa...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wang, Jianjun [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
10 |
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| Übergeordnetes Werk: |
Enthalten in: An Early Definition of Response to Corticosteroids in Acute Severe Autoimmune Hepatitis - Saffioti, F. ELSEVIER, 2016, Edinburgh |
|---|---|
| Übergeordnetes Werk: |
volume:95 ; year:2015 ; number:4 ; pages:505-514 ; extent:10 |
| Links: |
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| DOI / URN: |
10.1016/j.tube.2015.04.006 |
|---|
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ELV02870732X |
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| 245 | 1 | 4 | |a The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages |
| 264 | 1 | |c 2015transfer abstract | |
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| 520 | |a Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. | ||
| 520 | |a Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. | ||
| 650 | 7 | |a Cytokines |2 Elsevier | |
| 650 | 7 | |a Cytoskeleton |2 Elsevier | |
| 650 | 7 | |a Mycobacterium avium |2 Elsevier | |
| 650 | 7 | |a Fibroblast growth factor-2 |2 Elsevier | |
| 650 | 7 | |a Macrophage |2 Elsevier | |
| 700 | 1 | |a Wang, Zeyou |4 oth | |
| 700 | 1 | |a Yao, Yongliang |4 oth | |
| 700 | 1 | |a Wu, Jianhong |4 oth | |
| 700 | 1 | |a Tang, Xin |4 oth | |
| 700 | 1 | |a Gu, Tao |4 oth | |
| 700 | 1 | |a Li, Guangxin |4 oth | |
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10.1016/j.tube.2015.04.006 doi GBVA2015004000029.pica (DE-627)ELV02870732X (ELSEVIER)S1472-9792(14)20493-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Wang, Jianjun verfasserin aut The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Cytokines Elsevier Cytoskeleton Elsevier Mycobacterium avium Elsevier Fibroblast growth factor-2 Elsevier Macrophage Elsevier Wang, Zeyou oth Yao, Yongliang oth Wu, Jianhong oth Tang, Xin oth Gu, Tao oth Li, Guangxin oth Enthalten in Churchill Livingstone Saffioti, F. ELSEVIER An Early Definition of Response to Corticosteroids in Acute Severe Autoimmune Hepatitis 2016 Edinburgh (DE-627)ELV013806319 volume:95 year:2015 number:4 pages:505-514 extent:10 https://doi.org/10.1016/j.tube.2015.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_11 GBV_ILN_40 GBV_ILN_61 GBV_ILN_63 GBV_ILN_181 GBV_ILN_235 GBV_ILN_721 GBV_ILN_723 GBV_ILN_737 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2018 GBV_ILN_2046 GBV_ILN_2469 44.44 Parasitologie Medizin VZ AR 95 2015 4 505-514 10 045F 610 |
| spelling |
10.1016/j.tube.2015.04.006 doi GBVA2015004000029.pica (DE-627)ELV02870732X (ELSEVIER)S1472-9792(14)20493-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Wang, Jianjun verfasserin aut The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Cytokines Elsevier Cytoskeleton Elsevier Mycobacterium avium Elsevier Fibroblast growth factor-2 Elsevier Macrophage Elsevier Wang, Zeyou oth Yao, Yongliang oth Wu, Jianhong oth Tang, Xin oth Gu, Tao oth Li, Guangxin oth Enthalten in Churchill Livingstone Saffioti, F. ELSEVIER An Early Definition of Response to Corticosteroids in Acute Severe Autoimmune Hepatitis 2016 Edinburgh (DE-627)ELV013806319 volume:95 year:2015 number:4 pages:505-514 extent:10 https://doi.org/10.1016/j.tube.2015.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_11 GBV_ILN_40 GBV_ILN_61 GBV_ILN_63 GBV_ILN_181 GBV_ILN_235 GBV_ILN_721 GBV_ILN_723 GBV_ILN_737 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2018 GBV_ILN_2046 GBV_ILN_2469 44.44 Parasitologie Medizin VZ AR 95 2015 4 505-514 10 045F 610 |
| allfields_unstemmed |
10.1016/j.tube.2015.04.006 doi GBVA2015004000029.pica (DE-627)ELV02870732X (ELSEVIER)S1472-9792(14)20493-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Wang, Jianjun verfasserin aut The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Cytokines Elsevier Cytoskeleton Elsevier Mycobacterium avium Elsevier Fibroblast growth factor-2 Elsevier Macrophage Elsevier Wang, Zeyou oth Yao, Yongliang oth Wu, Jianhong oth Tang, Xin oth Gu, Tao oth Li, Guangxin oth Enthalten in Churchill Livingstone Saffioti, F. ELSEVIER An Early Definition of Response to Corticosteroids in Acute Severe Autoimmune Hepatitis 2016 Edinburgh (DE-627)ELV013806319 volume:95 year:2015 number:4 pages:505-514 extent:10 https://doi.org/10.1016/j.tube.2015.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_11 GBV_ILN_40 GBV_ILN_61 GBV_ILN_63 GBV_ILN_181 GBV_ILN_235 GBV_ILN_721 GBV_ILN_723 GBV_ILN_737 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2018 GBV_ILN_2046 GBV_ILN_2469 44.44 Parasitologie Medizin VZ AR 95 2015 4 505-514 10 045F 610 |
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10.1016/j.tube.2015.04.006 doi GBVA2015004000029.pica (DE-627)ELV02870732X (ELSEVIER)S1472-9792(14)20493-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Wang, Jianjun verfasserin aut The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Cytokines Elsevier Cytoskeleton Elsevier Mycobacterium avium Elsevier Fibroblast growth factor-2 Elsevier Macrophage Elsevier Wang, Zeyou oth Yao, Yongliang oth Wu, Jianhong oth Tang, Xin oth Gu, Tao oth Li, Guangxin oth Enthalten in Churchill Livingstone Saffioti, F. ELSEVIER An Early Definition of Response to Corticosteroids in Acute Severe Autoimmune Hepatitis 2016 Edinburgh (DE-627)ELV013806319 volume:95 year:2015 number:4 pages:505-514 extent:10 https://doi.org/10.1016/j.tube.2015.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_11 GBV_ILN_40 GBV_ILN_61 GBV_ILN_63 GBV_ILN_181 GBV_ILN_235 GBV_ILN_721 GBV_ILN_723 GBV_ILN_737 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2018 GBV_ILN_2046 GBV_ILN_2469 44.44 Parasitologie Medizin VZ AR 95 2015 4 505-514 10 045F 610 |
| allfieldsSound |
10.1016/j.tube.2015.04.006 doi GBVA2015004000029.pica (DE-627)ELV02870732X (ELSEVIER)S1472-9792(14)20493-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Wang, Jianjun verfasserin aut The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. Cytokines Elsevier Cytoskeleton Elsevier Mycobacterium avium Elsevier Fibroblast growth factor-2 Elsevier Macrophage Elsevier Wang, Zeyou oth Yao, Yongliang oth Wu, Jianhong oth Tang, Xin oth Gu, Tao oth Li, Guangxin oth Enthalten in Churchill Livingstone Saffioti, F. ELSEVIER An Early Definition of Response to Corticosteroids in Acute Severe Autoimmune Hepatitis 2016 Edinburgh (DE-627)ELV013806319 volume:95 year:2015 number:4 pages:505-514 extent:10 https://doi.org/10.1016/j.tube.2015.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_11 GBV_ILN_40 GBV_ILN_61 GBV_ILN_63 GBV_ILN_181 GBV_ILN_235 GBV_ILN_721 GBV_ILN_723 GBV_ILN_737 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2018 GBV_ILN_2046 GBV_ILN_2469 44.44 Parasitologie Medizin VZ AR 95 2015 4 505-514 10 045F 610 |
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The fibroblast growth factor-2 arrests Mycobacterium avium sp. paratuberculosis growth and immunomodulates host response in macrophages |
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Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. |
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Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. |
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Mycobacterium tuberculosisis (M. tb) epidemic is one of the most severe health problem worldwide, while mechanisms underlying its pathogenesis and host immune responses remain unclear. Mycobacterium avium (M. avium), a mycobacterial species related to M. tb, shares similarities with M. tb in many ways. In this study, using M. avium infection of macrophages as a model, we systematically studied the effect of fibroblast growth factor-2 (FGF-2) on M. avium infection of macrophages. Our results showed that M. avium infection could increase FGF-2 expression on both mRNA and protein levels. M. avium infection elevated TNF-α and IFN-γ production while the addition of FGF-2 could further increase TNF-α but not IFN-γ level. M. avium infection could increase the expression of oxygen/nitrogen metabolism proteins iNOS and SOD-1, and FGF-2 had additive effect on the expression of these two proteins. M. avium infection had inhibitive effect on actin expression while FGF-2 could partly counteract such inhibition. Moreover, FGF-2 could inhibit M. avium proliferation in macrophages. Our results together indicate that macrophage-secreted FGF-2 upon M. avium infection could suppress M. avium proliferation through various ways including cytokine production, enhancement of phagocytosis as well as oxygen/nitrogen metabolism. |
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