Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia

Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in...
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Autor*in:	Soichi Yamada [verfasserIn] Shion Miyoshi [verfasserIn] Junko Nishio [verfasserIn] Satoshi Mizutani [verfasserIn] Zento Yamada [verfasserIn] Natsuko Kusunoki [verfasserIn] Hiroshi Sato [verfasserIn] Yoshikazu Kuboi [verfasserIn] Kana Hoshino-Negishi [verfasserIn] Naoto Ishii [verfasserIn] Toshio Imai [verfasserIn] Tetsuo Mikami [verfasserIn] Hiroyasu Nakano [verfasserIn] Shinichi Kawai [verfasserIn] Toshihiro Nanki [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Übergeordnetes Werk:	In: European Journal of Inflammation - SAGE Publishing, 2017, 18(2020)
Übergeordnetes Werk:	volume:18 ; year:2020

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1177/2058739220959903

Katalog-ID:	DOAJ058500677

Internformat


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520			\|a Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP.
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700	0		\|a Satoshi Mizutani \|e verfasserin \|4 aut
700	0		\|a Zento Yamada \|e verfasserin \|4 aut
700	0		\|a Natsuko Kusunoki \|e verfasserin \|4 aut
700	0		\|a Hiroshi Sato \|e verfasserin \|4 aut
700	0		\|a Yoshikazu Kuboi \|e verfasserin \|4 aut
700	0		\|a Kana Hoshino-Negishi \|e verfasserin \|4 aut
700	0		\|a Naoto Ishii \|e verfasserin \|4 aut
700	0		\|a Toshio Imai \|e verfasserin \|4 aut
700	0		\|a Tetsuo Mikami \|e verfasserin \|4 aut
700	0		\|a Hiroyasu Nakano \|e verfasserin \|4 aut
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700	0		\|a Toshihiro Nanki \|e verfasserin \|4 aut
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952			\|d 18 \|j 2020

Indexfelder

author_variant	s y sy s m sm j n jn s m sm z y zy n k nk h s hs y k yk k h n khn n i ni t i ti t m tm h n hn s k sk t n tn
matchkey_str	article:20587392:2020----::fetoc3lihbtoomrnbemcnnuei
hierarchy_sort_str	2020
publishDate	2020
allfields	10.1177/2058739220959903 doi (DE-627)DOAJ058500677 (DE-599)DOAJ48e60c0fad3a48ec963e241e13797b31 DE-627 ger DE-627 rakwb eng Soichi Yamada verfasserin aut Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP. Medicine R Shion Miyoshi verfasserin aut Junko Nishio verfasserin aut Satoshi Mizutani verfasserin aut Zento Yamada verfasserin aut Natsuko Kusunoki verfasserin aut Hiroshi Sato verfasserin aut Yoshikazu Kuboi verfasserin aut Kana Hoshino-Negishi verfasserin aut Naoto Ishii verfasserin aut Toshio Imai verfasserin aut Tetsuo Mikami verfasserin aut Hiroyasu Nakano verfasserin aut Shinichi Kawai verfasserin aut Toshihiro Nanki verfasserin aut In European Journal of Inflammation SAGE Publishing, 2017 18(2020) (DE-627)641397232 (DE-600)2584683-8 20587392 nnns volume:18 year:2020 https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/article/48e60c0fad3a48ec963e241e13797b31 kostenfrei https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/toc/2058-7392 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2098 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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 18 2020
spelling	10.1177/2058739220959903 doi (DE-627)DOAJ058500677 (DE-599)DOAJ48e60c0fad3a48ec963e241e13797b31 DE-627 ger DE-627 rakwb eng Soichi Yamada verfasserin aut Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP. Medicine R Shion Miyoshi verfasserin aut Junko Nishio verfasserin aut Satoshi Mizutani verfasserin aut Zento Yamada verfasserin aut Natsuko Kusunoki verfasserin aut Hiroshi Sato verfasserin aut Yoshikazu Kuboi verfasserin aut Kana Hoshino-Negishi verfasserin aut Naoto Ishii verfasserin aut Toshio Imai verfasserin aut Tetsuo Mikami verfasserin aut Hiroyasu Nakano verfasserin aut Shinichi Kawai verfasserin aut Toshihiro Nanki verfasserin aut In European Journal of Inflammation SAGE Publishing, 2017 18(2020) (DE-627)641397232 (DE-600)2584683-8 20587392 nnns volume:18 year:2020 https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/article/48e60c0fad3a48ec963e241e13797b31 kostenfrei https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/toc/2058-7392 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2098 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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 18 2020
allfields_unstemmed	10.1177/2058739220959903 doi (DE-627)DOAJ058500677 (DE-599)DOAJ48e60c0fad3a48ec963e241e13797b31 DE-627 ger DE-627 rakwb eng Soichi Yamada verfasserin aut Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP. Medicine R Shion Miyoshi verfasserin aut Junko Nishio verfasserin aut Satoshi Mizutani verfasserin aut Zento Yamada verfasserin aut Natsuko Kusunoki verfasserin aut Hiroshi Sato verfasserin aut Yoshikazu Kuboi verfasserin aut Kana Hoshino-Negishi verfasserin aut Naoto Ishii verfasserin aut Toshio Imai verfasserin aut Tetsuo Mikami verfasserin aut Hiroyasu Nakano verfasserin aut Shinichi Kawai verfasserin aut Toshihiro Nanki verfasserin aut In European Journal of Inflammation SAGE Publishing, 2017 18(2020) (DE-627)641397232 (DE-600)2584683-8 20587392 nnns volume:18 year:2020 https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/article/48e60c0fad3a48ec963e241e13797b31 kostenfrei https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/toc/2058-7392 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2098 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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 18 2020
allfieldsGer	10.1177/2058739220959903 doi (DE-627)DOAJ058500677 (DE-599)DOAJ48e60c0fad3a48ec963e241e13797b31 DE-627 ger DE-627 rakwb eng Soichi Yamada verfasserin aut Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP. Medicine R Shion Miyoshi verfasserin aut Junko Nishio verfasserin aut Satoshi Mizutani verfasserin aut Zento Yamada verfasserin aut Natsuko Kusunoki verfasserin aut Hiroshi Sato verfasserin aut Yoshikazu Kuboi verfasserin aut Kana Hoshino-Negishi verfasserin aut Naoto Ishii verfasserin aut Toshio Imai verfasserin aut Tetsuo Mikami verfasserin aut Hiroyasu Nakano verfasserin aut Shinichi Kawai verfasserin aut Toshihiro Nanki verfasserin aut In European Journal of Inflammation SAGE Publishing, 2017 18(2020) (DE-627)641397232 (DE-600)2584683-8 20587392 nnns volume:18 year:2020 https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/article/48e60c0fad3a48ec963e241e13797b31 kostenfrei https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/toc/2058-7392 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2098 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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 18 2020
allfieldsSound	10.1177/2058739220959903 doi (DE-627)DOAJ058500677 (DE-599)DOAJ48e60c0fad3a48ec963e241e13797b31 DE-627 ger DE-627 rakwb eng Soichi Yamada verfasserin aut Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP. Medicine R Shion Miyoshi verfasserin aut Junko Nishio verfasserin aut Satoshi Mizutani verfasserin aut Zento Yamada verfasserin aut Natsuko Kusunoki verfasserin aut Hiroshi Sato verfasserin aut Yoshikazu Kuboi verfasserin aut Kana Hoshino-Negishi verfasserin aut Naoto Ishii verfasserin aut Toshio Imai verfasserin aut Tetsuo Mikami verfasserin aut Hiroyasu Nakano verfasserin aut Shinichi Kawai verfasserin aut Toshihiro Nanki verfasserin aut In European Journal of Inflammation SAGE Publishing, 2017 18(2020) (DE-627)641397232 (DE-600)2584683-8 20587392 nnns volume:18 year:2020 https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/article/48e60c0fad3a48ec963e241e13797b31 kostenfrei https://doi.org/10.1177/2058739220959903 kostenfrei https://doaj.org/toc/2058-7392 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2098 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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 18 2020
language	English
source	In European Journal of Inflammation 18(2020) volume:18 year:2020
sourceStr	In European Journal of Inflammation 18(2020) volume:18 year:2020
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Medicine R
isfreeaccess_bool	true
container_title	European Journal of Inflammation
authorswithroles_txt_mv	Soichi Yamada @@aut@@ Shion Miyoshi @@aut@@ Junko Nishio @@aut@@ Satoshi Mizutani @@aut@@ Zento Yamada @@aut@@ Natsuko Kusunoki @@aut@@ Hiroshi Sato @@aut@@ Yoshikazu Kuboi @@aut@@ Kana Hoshino-Negishi @@aut@@ Naoto Ishii @@aut@@ Toshio Imai @@aut@@ Tetsuo Mikami @@aut@@ Hiroyasu Nakano @@aut@@ Shinichi Kawai @@aut@@ Toshihiro Nanki @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	641397232
id	DOAJ058500677
language_de	englisch
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Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. 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author	Soichi Yamada
spellingShingle	Soichi Yamada misc Medicine misc R Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia
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topic_title	Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia
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title	Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia
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title_full	Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia
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journal	European Journal of Inflammation
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author_browse	Soichi Yamada Shion Miyoshi Junko Nishio Satoshi Mizutani Zento Yamada Natsuko Kusunoki Hiroshi Sato Yoshikazu Kuboi Kana Hoshino-Negishi Naoto Ishii Toshio Imai Tetsuo Mikami Hiroyasu Nakano Shinichi Kawai Toshihiro Nanki
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author-letter	Soichi Yamada
doi_str_mv	10.1177/2058739220959903
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title_sort	effects of cx3cl1 inhibition on murine bleomycin-induced interstitial pneumonia
title_auth	Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia
abstract	Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP.
abstractGer	Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP.
abstract_unstemmed	Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP.
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title_short	Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia
url	https://doi.org/10.1177/2058739220959903 https://doaj.org/article/48e60c0fad3a48ec963e241e13797b31 https://doaj.org/toc/2058-7392
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author2Str	Shion Miyoshi Junko Nishio Satoshi Mizutani Zento Yamada Natsuko Kusunoki Hiroshi Sato Yoshikazu Kuboi Kana Hoshino-Negishi Naoto Ishii Toshio Imai Tetsuo Mikami Hiroyasu Nakano Shinichi Kawai Toshihiro Nanki
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Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia

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