Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis
Purpose Ulcerative colitis (UC) is a chronic inflammatory disease of the colon that affects an increasing number of patients. High comorbidity is observed between UC and other diseases in which inflammation may be involved, including brain diseases such as cognitive impairment, mental disorders, anx...
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| creator | Kurtys, E. Doorduin, J. Eisel, U. L. M. Dierckx, R. A. J. O. de Vries, E. F. J. |
| description | Purpose
Ulcerative colitis (UC) is a chronic inflammatory disease of the colon that affects an increasing number of patients. High comorbidity is observed between UC and other diseases in which inflammation may be involved, including brain diseases such as cognitive impairment, mental disorders, anxiety, and depression. To investigate the increased occurrence of these brain diseases in patients with UC, non-invasive methods for monitoring peripheral and central inflammation could be applied. Therefore, the goal of this study is to assess the feasibility of monitoring gut and brain inflammation in a rat model of chemically induced colitis by positron emission tomography (PET) with [
11
C]PBR28, a tracer targeting the translocator protein (TSPO), which is upregulated when microglia and macrophages are activated.
Procedures
Colitis was induced in rats by intra-rectal injection of 2,4,6-trinitrobenzenesulfonic acid (TNBS). Rats with colitis and healthy control animals were subjected to [
11
C]PBR28 PET of the abdomen followed by
ex vivo
biodistribution in order to assess whether inflammation in the gut could be detected. Another group of rats with colitis underwent repetitive [
11
C]PBR28 PET imaging of the brain to investigate the development of neuroinflammation.
Results
Eleven days after TNBS injection,
ex vivo
biodistribution studies demonstrated increased [
11
C]PBR28 uptake in the inflamed cecum and colon of rats with colitis as compared to healthy controls, whereas PET imaging did not show any difference between groups at any time. Similarly, repetitive PET imaging of the brain did not reveal any neuroinflammation induced by the TNBS administration in the colon. In contrast, significantly increased [
11
C]PBR28 uptake in cerebellum could be detected in
ex vivo
biodistribution studies on day 11.
Conclusion
Inflammation in both the gut and the brain of rats with chemically induced colitis was observed by
ex vivo
biodistribution. However, these effects could not be detected by [
11
C]PBR28 PET imaging in our colitis model, which is likely due to spill-over effects and insufficient resolution of the PET camera. |
| doi_str_mv | 10.1007/s11307-016-0979-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5209392</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1859500094</sourcerecordid><originalsourceid>FETCH-LOGICAL-c503t-739a49ecfa3555fd0a1cf81d283a112bffeb70786d1c5fc3d1d64560965d64613</originalsourceid><addsrcrecordid>eNqNkVFrFTEQhRdRbK3-AF8k4IsvW2eSm2T3RbDLtS1ULKU-iYTc3aRNySa3yW6h_94st5YqCD5lwnznTDKnqt4iHCKA_JgRGcgaUNTQyraGZ9U-NgJqCkCfl5ozUaNgdK96lfMNAEqk7GW1R-UKKLR0v9qu77Sf9eTCFfmB2P08P7qgDTlfXxIbE_kag5tiWrrH80R0GMhR0i6Q02C9HscijIGUuyYXeir4YDyJlnTXZnS99v6-kMPcm4F00bvJ5dfVC6t9Nm8ezoPq-5f1ZXdSn307Pu0-n9U9BzbVkrV61ZreasY5twNo7G2DA22YRqQba81GgmzEgD23PRtwECsuoBW8FALZQfVp57udN6MZehOmpL3aJjfqdK-idurPTnDX6ireKV4Ww1paDD48GKR4O5s8qdHl3nivg4lzVtjwlgNAu_oPlAqJK85kQd__hd7EOYWyicWQAzYNXWbjjupTzDkZ-_huBLVEr3bRqxK9WqJXUDTvnn74UfE76wLQHZC3S6AmPRn9T9dfC1W3jQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1855018822</pqid></control><display><type>article</type><title>Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Kurtys, E. ; Doorduin, J. ; Eisel, U. L. M. ; Dierckx, R. A. J. O. ; de Vries, E. F. J.</creator><creatorcontrib>Kurtys, E. ; Doorduin, J. ; Eisel, U. L. M. ; Dierckx, R. A. J. O. ; de Vries, E. F. J.</creatorcontrib><description>Purpose
Ulcerative colitis (UC) is a chronic inflammatory disease of the colon that affects an increasing number of patients. High comorbidity is observed between UC and other diseases in which inflammation may be involved, including brain diseases such as cognitive impairment, mental disorders, anxiety, and depression. To investigate the increased occurrence of these brain diseases in patients with UC, non-invasive methods for monitoring peripheral and central inflammation could be applied. Therefore, the goal of this study is to assess the feasibility of monitoring gut and brain inflammation in a rat model of chemically induced colitis by positron emission tomography (PET) with [
11
C]PBR28, a tracer targeting the translocator protein (TSPO), which is upregulated when microglia and macrophages are activated.
Procedures
Colitis was induced in rats by intra-rectal injection of 2,4,6-trinitrobenzenesulfonic acid (TNBS). Rats with colitis and healthy control animals were subjected to [
11
C]PBR28 PET of the abdomen followed by
ex vivo
biodistribution in order to assess whether inflammation in the gut could be detected. Another group of rats with colitis underwent repetitive [
11
C]PBR28 PET imaging of the brain to investigate the development of neuroinflammation.
Results
Eleven days after TNBS injection,
ex vivo
biodistribution studies demonstrated increased [
11
C]PBR28 uptake in the inflamed cecum and colon of rats with colitis as compared to healthy controls, whereas PET imaging did not show any difference between groups at any time. Similarly, repetitive PET imaging of the brain did not reveal any neuroinflammation induced by the TNBS administration in the colon. In contrast, significantly increased [
11
C]PBR28 uptake in cerebellum could be detected in
ex vivo
biodistribution studies on day 11.
Conclusion
Inflammation in both the gut and the brain of rats with chemically induced colitis was observed by
ex vivo
biodistribution. However, these effects could not be detected by [
11
C]PBR28 PET imaging in our colitis model, which is likely due to spill-over effects and insufficient resolution of the PET camera.</description><identifier>ISSN: 1536-1632</identifier><identifier>EISSN: 1860-2002</identifier><identifier>DOI: 10.1007/s11307-016-0979-0</identifier><identifier>PMID: 27402092</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Abdomen - pathology ; Animals ; Colitis - chemically induced ; Colitis - diagnostic imaging ; Colitis - pathology ; Digestive System - diagnostic imaging ; Digestive System - pathology ; Disease Models, Animal ; Disease Progression ; Encephalitis - diagnostic imaging ; Encephalitis - pathology ; Imaging ; Medicine ; Medicine & Public Health ; Positron-Emission Tomography - methods ; Pyrimidines - chemistry ; Radiology ; Rats, Sprague-Dawley ; Research Article ; Tissue Distribution</subject><ispartof>Molecular imaging and biology, 2017-02, Vol.19 (1), p.68-76</ispartof><rights>The Author(s) 2016</rights><rights>Molecular Imaging and Biology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-739a49ecfa3555fd0a1cf81d283a112bffeb70786d1c5fc3d1d64560965d64613</citedby><cites>FETCH-LOGICAL-c503t-739a49ecfa3555fd0a1cf81d283a112bffeb70786d1c5fc3d1d64560965d64613</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11307-016-0979-0$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11307-016-0979-0$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,315,781,785,886,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27402092$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kurtys, E.</creatorcontrib><creatorcontrib>Doorduin, J.</creatorcontrib><creatorcontrib>Eisel, U. L. M.</creatorcontrib><creatorcontrib>Dierckx, R. A. J. O.</creatorcontrib><creatorcontrib>de Vries, E. F. J.</creatorcontrib><title>Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis</title><title>Molecular imaging and biology</title><addtitle>Mol Imaging Biol</addtitle><addtitle>Mol Imaging Biol</addtitle><description>Purpose
Ulcerative colitis (UC) is a chronic inflammatory disease of the colon that affects an increasing number of patients. High comorbidity is observed between UC and other diseases in which inflammation may be involved, including brain diseases such as cognitive impairment, mental disorders, anxiety, and depression. To investigate the increased occurrence of these brain diseases in patients with UC, non-invasive methods for monitoring peripheral and central inflammation could be applied. Therefore, the goal of this study is to assess the feasibility of monitoring gut and brain inflammation in a rat model of chemically induced colitis by positron emission tomography (PET) with [
11
C]PBR28, a tracer targeting the translocator protein (TSPO), which is upregulated when microglia and macrophages are activated.
Procedures
Colitis was induced in rats by intra-rectal injection of 2,4,6-trinitrobenzenesulfonic acid (TNBS). Rats with colitis and healthy control animals were subjected to [
11
C]PBR28 PET of the abdomen followed by
ex vivo
biodistribution in order to assess whether inflammation in the gut could be detected. Another group of rats with colitis underwent repetitive [
11
C]PBR28 PET imaging of the brain to investigate the development of neuroinflammation.
Results
Eleven days after TNBS injection,
ex vivo
biodistribution studies demonstrated increased [
11
C]PBR28 uptake in the inflamed cecum and colon of rats with colitis as compared to healthy controls, whereas PET imaging did not show any difference between groups at any time. Similarly, repetitive PET imaging of the brain did not reveal any neuroinflammation induced by the TNBS administration in the colon. In contrast, significantly increased [
11
C]PBR28 uptake in cerebellum could be detected in
ex vivo
biodistribution studies on day 11.
Conclusion
Inflammation in both the gut and the brain of rats with chemically induced colitis was observed by
ex vivo
biodistribution. However, these effects could not be detected by [
11
C]PBR28 PET imaging in our colitis model, which is likely due to spill-over effects and insufficient resolution of the PET camera.</description><subject>Abdomen - pathology</subject><subject>Animals</subject><subject>Colitis - chemically induced</subject><subject>Colitis - diagnostic imaging</subject><subject>Colitis - pathology</subject><subject>Digestive System - diagnostic imaging</subject><subject>Digestive System - pathology</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Encephalitis - diagnostic imaging</subject><subject>Encephalitis - pathology</subject><subject>Imaging</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Positron-Emission Tomography - methods</subject><subject>Pyrimidines - chemistry</subject><subject>Radiology</subject><subject>Rats, Sprague-Dawley</subject><subject>Research Article</subject><subject>Tissue Distribution</subject><issn>1536-1632</issn><issn>1860-2002</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkVFrFTEQhRdRbK3-AF8k4IsvW2eSm2T3RbDLtS1ULKU-iYTc3aRNySa3yW6h_94st5YqCD5lwnznTDKnqt4iHCKA_JgRGcgaUNTQyraGZ9U-NgJqCkCfl5ozUaNgdK96lfMNAEqk7GW1R-UKKLR0v9qu77Sf9eTCFfmB2P08P7qgDTlfXxIbE_kag5tiWrrH80R0GMhR0i6Q02C9HscijIGUuyYXeir4YDyJlnTXZnS99v6-kMPcm4F00bvJ5dfVC6t9Nm8ezoPq-5f1ZXdSn307Pu0-n9U9BzbVkrV61ZreasY5twNo7G2DA22YRqQba81GgmzEgD23PRtwECsuoBW8FALZQfVp57udN6MZehOmpL3aJjfqdK-idurPTnDX6ireKV4Ww1paDD48GKR4O5s8qdHl3nivg4lzVtjwlgNAu_oPlAqJK85kQd__hd7EOYWyicWQAzYNXWbjjupTzDkZ-_huBLVEr3bRqxK9WqJXUDTvnn74UfE76wLQHZC3S6AmPRn9T9dfC1W3jQ</recordid><startdate>20170201</startdate><enddate>20170201</enddate><creator>Kurtys, E.</creator><creator>Doorduin, J.</creator><creator>Eisel, U. L. M.</creator><creator>Dierckx, R. A. J. O.</creator><creator>de Vries, E. F. J.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>L6V</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170201</creationdate><title>Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis</title><author>Kurtys, E. ; Doorduin, J. ; Eisel, U. L. M. ; Dierckx, R. A. J. O. ; de Vries, E. F. J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-739a49ecfa3555fd0a1cf81d283a112bffeb70786d1c5fc3d1d64560965d64613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Abdomen - pathology</topic><topic>Animals</topic><topic>Colitis - chemically induced</topic><topic>Colitis - diagnostic imaging</topic><topic>Colitis - pathology</topic><topic>Digestive System - diagnostic imaging</topic><topic>Digestive System - pathology</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Encephalitis - diagnostic imaging</topic><topic>Encephalitis - pathology</topic><topic>Imaging</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Positron-Emission Tomography - methods</topic><topic>Pyrimidines - chemistry</topic><topic>Radiology</topic><topic>Rats, Sprague-Dawley</topic><topic>Research Article</topic><topic>Tissue Distribution</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kurtys, E.</creatorcontrib><creatorcontrib>Doorduin, J.</creatorcontrib><creatorcontrib>Eisel, U. L. M.</creatorcontrib><creatorcontrib>Dierckx, R. A. J. O.</creatorcontrib><creatorcontrib>de Vries, E. F. J.</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular imaging and biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kurtys, E.</au><au>Doorduin, J.</au><au>Eisel, U. L. M.</au><au>Dierckx, R. A. J. O.</au><au>de Vries, E. F. J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis</atitle><jtitle>Molecular imaging and biology</jtitle><stitle>Mol Imaging Biol</stitle><addtitle>Mol Imaging Biol</addtitle><date>2017-02-01</date><risdate>2017</risdate><volume>19</volume><issue>1</issue><spage>68</spage><epage>76</epage><pages>68-76</pages><issn>1536-1632</issn><eissn>1860-2002</eissn><abstract>Purpose
Ulcerative colitis (UC) is a chronic inflammatory disease of the colon that affects an increasing number of patients. High comorbidity is observed between UC and other diseases in which inflammation may be involved, including brain diseases such as cognitive impairment, mental disorders, anxiety, and depression. To investigate the increased occurrence of these brain diseases in patients with UC, non-invasive methods for monitoring peripheral and central inflammation could be applied. Therefore, the goal of this study is to assess the feasibility of monitoring gut and brain inflammation in a rat model of chemically induced colitis by positron emission tomography (PET) with [
11
C]PBR28, a tracer targeting the translocator protein (TSPO), which is upregulated when microglia and macrophages are activated.
Procedures
Colitis was induced in rats by intra-rectal injection of 2,4,6-trinitrobenzenesulfonic acid (TNBS). Rats with colitis and healthy control animals were subjected to [
11
C]PBR28 PET of the abdomen followed by
ex vivo
biodistribution in order to assess whether inflammation in the gut could be detected. Another group of rats with colitis underwent repetitive [
11
C]PBR28 PET imaging of the brain to investigate the development of neuroinflammation.
Results
Eleven days after TNBS injection,
ex vivo
biodistribution studies demonstrated increased [
11
C]PBR28 uptake in the inflamed cecum and colon of rats with colitis as compared to healthy controls, whereas PET imaging did not show any difference between groups at any time. Similarly, repetitive PET imaging of the brain did not reveal any neuroinflammation induced by the TNBS administration in the colon. In contrast, significantly increased [
11
C]PBR28 uptake in cerebellum could be detected in
ex vivo
biodistribution studies on day 11.
Conclusion
Inflammation in both the gut and the brain of rats with chemically induced colitis was observed by
ex vivo
biodistribution. However, these effects could not be detected by [
11
C]PBR28 PET imaging in our colitis model, which is likely due to spill-over effects and insufficient resolution of the PET camera.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27402092</pmid><doi>10.1007/s11307-016-0979-0</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Molecular imaging and biology, 2017-02, Vol.19 (1), p.68-76 |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Abdomen - pathology Animals Colitis - chemically induced Colitis - diagnostic imaging Colitis - pathology Digestive System - diagnostic imaging Digestive System - pathology Disease Models, Animal Disease Progression Encephalitis - diagnostic imaging Encephalitis - pathology Imaging Medicine Medicine & Public Health Positron-Emission Tomography - methods Pyrimidines - chemistry Radiology Rats, Sprague-Dawley Research Article Tissue Distribution |
| title | Evaluating [11C]PBR28 PET for Monitoring Gut and Brain Inflammation in a Rat Model of Chemically Induced Colitis |
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