Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis
The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemica...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sarashina-Kida, Hana [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 114(2017), 38, Seite 10178 |
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| Übergeordnetes Werk: |
volume:114 ; year:2017 ; number:38 ; pages:10178 |
| Links: |
|---|
| DOI / URN: |
10.1073/pnas.1712837114 |
|---|
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OLC199853782X |
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| 520 | |a The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. | ||
| 650 | 4 | |a Surfactant protein D | |
| 650 | 4 | |a Microbiota (Symbiotic organisms) | |
| 650 | 4 | |a Physiological aspects | |
| 650 | 4 | |a Immunoregulation | |
| 650 | 4 | |a Synthesis (chemistry) | |
| 650 | 4 | |a Homeostasis | |
| 650 | 4 | |a Gene expression | |
| 650 | 4 | |a Inflammatory diseases | |
| 650 | 4 | |a Gnotobiotics | |
| 650 | 4 | |a Dysbacteriosis | |
| 650 | 4 | |a Dextran | |
| 650 | 4 | |a Bacteria | |
| 650 | 4 | |a Mice | |
| 650 | 4 | |a Studies | |
| 650 | 4 | |a Cholecystectomy | |
| 650 | 4 | |a Glucocorticoids | |
| 650 | 4 | |a Organs | |
| 650 | 4 | |a Sulfate | |
| 650 | 4 | |a Sodium | |
| 650 | 4 | |a Gallbladder | |
| 650 | 4 | |a Digestive tract | |
| 650 | 4 | |a Dextran sulfate | |
| 650 | 4 | |a Protein D | |
| 650 | 4 | |a Lung | |
| 650 | 4 | |a Liver | |
| 650 | 4 | |a Intestine | |
| 650 | 4 | |a Proteins | |
| 650 | 4 | |a Gastrointestinal tract | |
| 650 | 4 | |a Surfactants | |
| 650 | 4 | |a Digestive system | |
| 650 | 4 | |a Colitis | |
| 700 | 1 | |a Negishi, Hideo |4 oth | |
| 700 | 1 | |a Nishio, Junko |4 oth | |
| 700 | 1 | |a Suda, Wataru |4 oth | |
| 700 | 1 | |a Nakajima, Yuki |4 oth | |
| 700 | 1 | |a Yasui-Kato, Mika |4 oth | |
| 700 | 1 | |a Iwaisako, Keiko |4 oth | |
| 700 | 1 | |a Kang, Sujin |4 oth | |
| 700 | 1 | |a Endo, Nobuyasu |4 oth | |
| 700 | 1 | |a Yanai, Hideyuki |4 oth | |
| 700 | 1 | |a Asagiri, Masataka |4 oth | |
| 700 | 1 | |a Kida, Hiroshi |4 oth | |
| 700 | 1 | |a Hattori, Masahira |4 oth | |
| 700 | 1 | |a Kumanogoh, Atsushi |4 oth | |
| 700 | 1 | |a Taniguchi, Tadatsugu |4 oth | |
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10.1073/pnas.1712837114 doi PQ20171228 (DE-627)OLC199853782X (DE-599)GBVOLC199853782X (PRQ)g1168-29cc67af8ce370531a0a5bddaba4b3dca1a34ffad1ad9ed231791c4efcf6587f0 (KEY)0583363920170000114003810178gallbladderderivedsurfactantproteindregulatesgutco DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Sarashina-Kida, Hana verfasserin aut Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. Surfactant protein D Microbiota (Symbiotic organisms) Physiological aspects Immunoregulation Synthesis (chemistry) Homeostasis Gene expression Inflammatory diseases Gnotobiotics Dysbacteriosis Dextran Bacteria Mice Studies Cholecystectomy Glucocorticoids Organs Sulfate Sodium Gallbladder Digestive tract Dextran sulfate Protein D Lung Liver Intestine Proteins Gastrointestinal tract Surfactants Digestive system Colitis Negishi, Hideo oth Nishio, Junko oth Suda, Wataru oth Nakajima, Yuki oth Yasui-Kato, Mika oth Iwaisako, Keiko oth Kang, Sujin oth Endo, Nobuyasu oth Yanai, Hideyuki oth Asagiri, Masataka oth Kida, Hiroshi oth Hattori, Masahira oth Kumanogoh, Atsushi oth Taniguchi, Tadatsugu oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 38, Seite 10178 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:38 pages:10178 http://dx.doi.org/10.1073/pnas.1712837114 Volltext https://search.proquest.com/docview/1946454091 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 38 10178 |
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10.1073/pnas.1712837114 doi PQ20171228 (DE-627)OLC199853782X (DE-599)GBVOLC199853782X (PRQ)g1168-29cc67af8ce370531a0a5bddaba4b3dca1a34ffad1ad9ed231791c4efcf6587f0 (KEY)0583363920170000114003810178gallbladderderivedsurfactantproteindregulatesgutco DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Sarashina-Kida, Hana verfasserin aut Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. Surfactant protein D Microbiota (Symbiotic organisms) Physiological aspects Immunoregulation Synthesis (chemistry) Homeostasis Gene expression Inflammatory diseases Gnotobiotics Dysbacteriosis Dextran Bacteria Mice Studies Cholecystectomy Glucocorticoids Organs Sulfate Sodium Gallbladder Digestive tract Dextran sulfate Protein D Lung Liver Intestine Proteins Gastrointestinal tract Surfactants Digestive system Colitis Negishi, Hideo oth Nishio, Junko oth Suda, Wataru oth Nakajima, Yuki oth Yasui-Kato, Mika oth Iwaisako, Keiko oth Kang, Sujin oth Endo, Nobuyasu oth Yanai, Hideyuki oth Asagiri, Masataka oth Kida, Hiroshi oth Hattori, Masahira oth Kumanogoh, Atsushi oth Taniguchi, Tadatsugu oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 38, Seite 10178 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:38 pages:10178 http://dx.doi.org/10.1073/pnas.1712837114 Volltext https://search.proquest.com/docview/1946454091 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 38 10178 |
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10.1073/pnas.1712837114 doi PQ20171228 (DE-627)OLC199853782X (DE-599)GBVOLC199853782X (PRQ)g1168-29cc67af8ce370531a0a5bddaba4b3dca1a34ffad1ad9ed231791c4efcf6587f0 (KEY)0583363920170000114003810178gallbladderderivedsurfactantproteindregulatesgutco DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Sarashina-Kida, Hana verfasserin aut Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. Surfactant protein D Microbiota (Symbiotic organisms) Physiological aspects Immunoregulation Synthesis (chemistry) Homeostasis Gene expression Inflammatory diseases Gnotobiotics Dysbacteriosis Dextran Bacteria Mice Studies Cholecystectomy Glucocorticoids Organs Sulfate Sodium Gallbladder Digestive tract Dextran sulfate Protein D Lung Liver Intestine Proteins Gastrointestinal tract Surfactants Digestive system Colitis Negishi, Hideo oth Nishio, Junko oth Suda, Wataru oth Nakajima, Yuki oth Yasui-Kato, Mika oth Iwaisako, Keiko oth Kang, Sujin oth Endo, Nobuyasu oth Yanai, Hideyuki oth Asagiri, Masataka oth Kida, Hiroshi oth Hattori, Masahira oth Kumanogoh, Atsushi oth Taniguchi, Tadatsugu oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 38, Seite 10178 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:38 pages:10178 http://dx.doi.org/10.1073/pnas.1712837114 Volltext https://search.proquest.com/docview/1946454091 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 38 10178 |
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10.1073/pnas.1712837114 doi PQ20171228 (DE-627)OLC199853782X (DE-599)GBVOLC199853782X (PRQ)g1168-29cc67af8ce370531a0a5bddaba4b3dca1a34ffad1ad9ed231791c4efcf6587f0 (KEY)0583363920170000114003810178gallbladderderivedsurfactantproteindregulatesgutco DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Sarashina-Kida, Hana verfasserin aut Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. Surfactant protein D Microbiota (Symbiotic organisms) Physiological aspects Immunoregulation Synthesis (chemistry) Homeostasis Gene expression Inflammatory diseases Gnotobiotics Dysbacteriosis Dextran Bacteria Mice Studies Cholecystectomy Glucocorticoids Organs Sulfate Sodium Gallbladder Digestive tract Dextran sulfate Protein D Lung Liver Intestine Proteins Gastrointestinal tract Surfactants Digestive system Colitis Negishi, Hideo oth Nishio, Junko oth Suda, Wataru oth Nakajima, Yuki oth Yasui-Kato, Mika oth Iwaisako, Keiko oth Kang, Sujin oth Endo, Nobuyasu oth Yanai, Hideyuki oth Asagiri, Masataka oth Kida, Hiroshi oth Hattori, Masahira oth Kumanogoh, Atsushi oth Taniguchi, Tadatsugu oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 38, Seite 10178 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:38 pages:10178 http://dx.doi.org/10.1073/pnas.1712837114 Volltext https://search.proquest.com/docview/1946454091 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 38 10178 |
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10.1073/pnas.1712837114 doi PQ20171228 (DE-627)OLC199853782X (DE-599)GBVOLC199853782X (PRQ)g1168-29cc67af8ce370531a0a5bddaba4b3dca1a34ffad1ad9ed231791c4efcf6587f0 (KEY)0583363920170000114003810178gallbladderderivedsurfactantproteindregulatesgutco DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Sarashina-Kida, Hana verfasserin aut Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. Surfactant protein D Microbiota (Symbiotic organisms) Physiological aspects Immunoregulation Synthesis (chemistry) Homeostasis Gene expression Inflammatory diseases Gnotobiotics Dysbacteriosis Dextran Bacteria Mice Studies Cholecystectomy Glucocorticoids Organs Sulfate Sodium Gallbladder Digestive tract Dextran sulfate Protein D Lung Liver Intestine Proteins Gastrointestinal tract Surfactants Digestive system Colitis Negishi, Hideo oth Nishio, Junko oth Suda, Wataru oth Nakajima, Yuki oth Yasui-Kato, Mika oth Iwaisako, Keiko oth Kang, Sujin oth Endo, Nobuyasu oth Yanai, Hideyuki oth Asagiri, Masataka oth Kida, Hiroshi oth Hattori, Masahira oth Kumanogoh, Atsushi oth Taniguchi, Tadatsugu oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 38, Seite 10178 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:38 pages:10178 http://dx.doi.org/10.1073/pnas.1712837114 Volltext https://search.proquest.com/docview/1946454091 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 38 10178 |
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Sarashina-Kida, Hana @@aut@@ Negishi, Hideo @@oth@@ Nishio, Junko @@oth@@ Suda, Wataru @@oth@@ Nakajima, Yuki @@oth@@ Yasui-Kato, Mika @@oth@@ Iwaisako, Keiko @@oth@@ Kang, Sujin @@oth@@ Endo, Nobuyasu @@oth@@ Yanai, Hideyuki @@oth@@ Asagiri, Masataka @@oth@@ Kida, Hiroshi @@oth@@ Hattori, Masahira @@oth@@ Kumanogoh, Atsushi @@oth@@ Taniguchi, Tadatsugu @@oth@@ |
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Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis |
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The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. |
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The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. |
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The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy. |
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Negishi, Hideo Nishio, Junko Suda, Wataru Nakajima, Yuki Yasui-Kato, Mika Iwaisako, Keiko Kang, Sujin Endo, Nobuyasu Yanai, Hideyuki Asagiri, Masataka Kida, Hiroshi Hattori, Masahira Kumanogoh, Atsushi Taniguchi, Tadatsugu |
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These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Surfactant protein D</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Microbiota (Symbiotic organisms)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Physiological aspects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immunoregulation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Synthesis (chemistry)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Homeostasis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gene expression</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Inflammatory diseases</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gnotobiotics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Dysbacteriosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Dextran</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Bacteria</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mice</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Studies</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cholecystectomy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Glucocorticoids</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Organs</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Sulfate</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield 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