Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease
Development of inflammatory bowel disease (IBD) involves the interplay of environmental and genetic factors with the host immune system. Mechanisms contributing to immune dysregulation in IBD are not fully defined. Development of novel therapeutic strategies is focused on controlling aberrant immune...
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| Veröffentlicht in: | PloS one 2013-10, Vol.8 (10), p.e76969-e76969 |
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| creator | Sena, Angela Grishina, Irina Thai, Anne Goulart, Larissa Macal, Monica Fenton, Anne Li, Jay Prindiville, Thomas Oliani, Sonia Maria Dandekar, Satya Goulart, Luiz Sankaran-Walters, Sumathi |
| description | Development of inflammatory bowel disease (IBD) involves the interplay of environmental and genetic factors with the host immune system. Mechanisms contributing to immune dysregulation in IBD are not fully defined. Development of novel therapeutic strategies is focused on controlling aberrant immune response in IBD. Current IBD therapy utilizes a combination of immunomodulators and biologics to suppress pro-inflammatory effectors of IBD. However, the role of immunomodulatory factors such as annexin A1 (ANXA1) is not well understood. The goal of this study was to examine the association between ANXA1 and IBD, and the effects of anti-TNF-α, Infliximab (IFX), therapy on ANXA1 expression.
ANXA1 and TNF-α transcript levels in PBMC were measured by RT PCR. Clinical follow up included the administration of serial ibdQs. ANXA1 expression in the gut mucosa was measured by IHC. Plasma ANXA1 levels were measured by ELISA.
We found that the reduction in ANXA1 protein levels in plasma coincided with a decrease in the ANXA1 mRNA expression in peripheral blood of IBD patients. ANXA1 expression is upregulated during IFX therapy in patients with a successful intervention but not in clinical non-responders. The IFX therapy also modified the cellular immune activation in the peripheral blood of IBD patients. Decreased expression of ANXA1 was detected in the colonic mucosa of IBD patients with incomplete resolution of inflammation during continuous therapy, which correlated with increased levels of TNF-α transcripts. Gut mucosal epithelial barrier disruption was evident by increased plasma bacterial 16S levels.
Loss of ANXA1 expression may support inflammation during IBD and can serve as a biomarker of disease progression. Changes in ANXA1 levels may be predictive of therapeutic efficacy. |
| doi_str_mv | 10.1371/journal.pone.0076969 |
| format | Article |
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ANXA1 and TNF-α transcript levels in PBMC were measured by RT PCR. Clinical follow up included the administration of serial ibdQs. ANXA1 expression in the gut mucosa was measured by IHC. Plasma ANXA1 levels were measured by ELISA.
We found that the reduction in ANXA1 protein levels in plasma coincided with a decrease in the ANXA1 mRNA expression in peripheral blood of IBD patients. ANXA1 expression is upregulated during IFX therapy in patients with a successful intervention but not in clinical non-responders. The IFX therapy also modified the cellular immune activation in the peripheral blood of IBD patients. Decreased expression of ANXA1 was detected in the colonic mucosa of IBD patients with incomplete resolution of inflammation during continuous therapy, which correlated with increased levels of TNF-α transcripts. Gut mucosal epithelial barrier disruption was evident by increased plasma bacterial 16S levels.
Loss of ANXA1 expression may support inflammation during IBD and can serve as a biomarker of disease progression. Changes in ANXA1 levels may be predictive of therapeutic efficacy.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0076969</identifier><identifier>PMID: 24130820</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Aged ; Annexin A1 - blood ; Annexin A1 - genetics ; Annexin A1 - metabolism ; Annexins ; Anti-inflammatory agents ; Antibodies, Monoclonal - pharmacology ; Antibodies, Monoclonal - therapeutic use ; Arthritis ; Biochemistry ; Biological effects ; Biomarkers ; Biopsy ; Blood ; Crohn Disease - blood ; Crohn Disease - drug therapy ; Crohn Disease - immunology ; Crohn Disease - metabolism ; Crohn's disease ; Crohns disease ; Development and progression ; Disease Progression ; DNA, Bacterial - blood ; DNA, Ribosomal - blood ; Enzyme-linked immunosorbent assay ; Female ; Gastroenterology ; Gene expression ; Gene Expression Regulation ; Genetic factors ; Health aspects ; Hepatology ; Humans ; Immune response ; Immune system ; Immunology ; Immunomodulation ; Immunomodulators ; Inflammation ; Inflammation - genetics ; Inflammation - metabolism ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Infliximab ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - metabolism ; Intestine ; Laboratories ; Lymphocyte Activation - drug effects ; Male ; Middle Aged ; Monoclonal antibodies ; Mucosa ; Neutrophils ; Patients ; Peripheral blood mononuclear cells ; Proteins ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Studies ; T-Lymphocytes - drug effects ; T-Lymphocytes - immunology ; Therapy ; Transcription ; Treatment Outcome ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Young Adult</subject><ispartof>PloS one, 2013-10, Vol.8 (10), p.e76969-e76969</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Sena et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Sena et al 2013 Sena et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-28115b982e6071fa6e02cd9c0265c4eb6e6fe9785e90e65972f3981eadc02f9e3</citedby><cites>FETCH-LOGICAL-c692t-28115b982e6071fa6e02cd9c0265c4eb6e6fe9785e90e65972f3981eadc02f9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794972/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794972/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24130820$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Foligne, Benoit</contributor><creatorcontrib>Sena, Angela</creatorcontrib><creatorcontrib>Grishina, Irina</creatorcontrib><creatorcontrib>Thai, Anne</creatorcontrib><creatorcontrib>Goulart, Larissa</creatorcontrib><creatorcontrib>Macal, Monica</creatorcontrib><creatorcontrib>Fenton, Anne</creatorcontrib><creatorcontrib>Li, Jay</creatorcontrib><creatorcontrib>Prindiville, Thomas</creatorcontrib><creatorcontrib>Oliani, Sonia Maria</creatorcontrib><creatorcontrib>Dandekar, Satya</creatorcontrib><creatorcontrib>Goulart, Luiz</creatorcontrib><creatorcontrib>Sankaran-Walters, Sumathi</creatorcontrib><title>Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Development of inflammatory bowel disease (IBD) involves the interplay of environmental and genetic factors with the host immune system. Mechanisms contributing to immune dysregulation in IBD are not fully defined. Development of novel therapeutic strategies is focused on controlling aberrant immune response in IBD. Current IBD therapy utilizes a combination of immunomodulators and biologics to suppress pro-inflammatory effectors of IBD. However, the role of immunomodulatory factors such as annexin A1 (ANXA1) is not well understood. The goal of this study was to examine the association between ANXA1 and IBD, and the effects of anti-TNF-α, Infliximab (IFX), therapy on ANXA1 expression.
ANXA1 and TNF-α transcript levels in PBMC were measured by RT PCR. Clinical follow up included the administration of serial ibdQs. ANXA1 expression in the gut mucosa was measured by IHC. Plasma ANXA1 levels were measured by ELISA.
We found that the reduction in ANXA1 protein levels in plasma coincided with a decrease in the ANXA1 mRNA expression in peripheral blood of IBD patients. ANXA1 expression is upregulated during IFX therapy in patients with a successful intervention but not in clinical non-responders. The IFX therapy also modified the cellular immune activation in the peripheral blood of IBD patients. Decreased expression of ANXA1 was detected in the colonic mucosa of IBD patients with incomplete resolution of inflammation during continuous therapy, which correlated with increased levels of TNF-α transcripts. Gut mucosal epithelial barrier disruption was evident by increased plasma bacterial 16S levels.
Loss of ANXA1 expression may support inflammation during IBD and can serve as a biomarker of disease progression. Changes in ANXA1 levels may be predictive of therapeutic efficacy.</description><subject>Adult</subject><subject>Aged</subject><subject>Annexin A1 - blood</subject><subject>Annexin A1 - genetics</subject><subject>Annexin A1 - metabolism</subject><subject>Annexins</subject><subject>Anti-inflammatory agents</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Arthritis</subject><subject>Biochemistry</subject><subject>Biological effects</subject><subject>Biomarkers</subject><subject>Biopsy</subject><subject>Blood</subject><subject>Crohn Disease - blood</subject><subject>Crohn Disease - drug therapy</subject><subject>Crohn Disease - immunology</subject><subject>Crohn Disease - metabolism</subject><subject>Crohn's disease</subject><subject>Crohns disease</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>DNA, Bacterial - blood</subject><subject>DNA, Ribosomal - blood</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Gastroenterology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genetic factors</subject><subject>Health aspects</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Immunomodulation</subject><subject>Immunomodulators</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Infliximab</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestine</subject><subject>Laboratories</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Monoclonal antibodies</subject><subject>Mucosa</subject><subject>Neutrophils</subject><subject>Patients</subject><subject>Peripheral blood mononuclear cells</subject><subject>Proteins</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Studies</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - immunology</subject><subject>Therapy</subject><subject>Transcription</subject><subject>Treatment Outcome</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Young Adult</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1r2zAUhs3YWLtu_2BshsHoLpLpy7J1MwhptwUKhX30VijykaNgW5lkl-TfT0ncEo9eDF1IOnrOe6SjN0neYjTFNMef1673raqnG9fCFKGcCy6eJedYUDLhBNHnJ-uz5FUIa4QyWnD-MjkjDFNUEHSe3F3tgoeqr1VnXZs6k6q2sxPbmlo1jeqc38VIC1vbpjOcwnbjIYQ9GgMb76rD9h7SuXerNqRXNoAK8Dp5YVQd4M0wXyS_v17_mn-f3Nx-W8xnNxPNBekmpMA4W4qCAEc5NooDIroUGhGeaQZLDtyAyIsMBAKeiZwYKgoMqoyIEUAvkvdH3U3tghxaEiRmDEdtlOWRWByJ0qm13HjbKL-TTll5CDhfSeU7q2uQhuUaTImAKc2IQAIQpiQTJisFNUxFrS9DtX7ZQKmh7byqR6Ljk9auZOXuJc0Fi5ePApeDgHd_egidbGzQUNeqBdcf7k2FKLgoIvrhH_Tp1w1UpeID4q-5WFfvReWM5QWlGUMiUtMnqDhKaKyO_jE2xkcJn0YJkelg21WqD0Eufv74f_b2bsx-PGFXoOpuFVzd770XxiA7gtq7EA1qHpuMkdzb_6Ebcm9_Odg_pr07_aDHpAe_078NYf_t</recordid><startdate>20131010</startdate><enddate>20131010</enddate><creator>Sena, Angela</creator><creator>Grishina, Irina</creator><creator>Thai, Anne</creator><creator>Goulart, Larissa</creator><creator>Macal, Monica</creator><creator>Fenton, Anne</creator><creator>Li, Jay</creator><creator>Prindiville, Thomas</creator><creator>Oliani, Sonia Maria</creator><creator>Dandekar, Satya</creator><creator>Goulart, Luiz</creator><creator>Sankaran-Walters, Sumathi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131010</creationdate><title>Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease</title><author>Sena, Angela ; Grishina, Irina ; Thai, Anne ; Goulart, Larissa ; Macal, Monica ; Fenton, Anne ; Li, Jay ; Prindiville, Thomas ; Oliani, Sonia Maria ; Dandekar, Satya ; Goulart, Luiz ; Sankaran-Walters, Sumathi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-28115b982e6071fa6e02cd9c0265c4eb6e6fe9785e90e65972f3981eadc02f9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Annexin A1 - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</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>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sena, Angela</au><au>Grishina, Irina</au><au>Thai, Anne</au><au>Goulart, Larissa</au><au>Macal, Monica</au><au>Fenton, Anne</au><au>Li, Jay</au><au>Prindiville, Thomas</au><au>Oliani, Sonia Maria</au><au>Dandekar, Satya</au><au>Goulart, Luiz</au><au>Sankaran-Walters, Sumathi</au><au>Foligne, Benoit</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-10-10</date><risdate>2013</risdate><volume>8</volume><issue>10</issue><spage>e76969</spage><epage>e76969</epage><pages>e76969-e76969</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Development of inflammatory bowel disease (IBD) involves the interplay of environmental and genetic factors with the host immune system. Mechanisms contributing to immune dysregulation in IBD are not fully defined. Development of novel therapeutic strategies is focused on controlling aberrant immune response in IBD. Current IBD therapy utilizes a combination of immunomodulators and biologics to suppress pro-inflammatory effectors of IBD. However, the role of immunomodulatory factors such as annexin A1 (ANXA1) is not well understood. The goal of this study was to examine the association between ANXA1 and IBD, and the effects of anti-TNF-α, Infliximab (IFX), therapy on ANXA1 expression.
ANXA1 and TNF-α transcript levels in PBMC were measured by RT PCR. Clinical follow up included the administration of serial ibdQs. ANXA1 expression in the gut mucosa was measured by IHC. Plasma ANXA1 levels were measured by ELISA.
We found that the reduction in ANXA1 protein levels in plasma coincided with a decrease in the ANXA1 mRNA expression in peripheral blood of IBD patients. ANXA1 expression is upregulated during IFX therapy in patients with a successful intervention but not in clinical non-responders. The IFX therapy also modified the cellular immune activation in the peripheral blood of IBD patients. Decreased expression of ANXA1 was detected in the colonic mucosa of IBD patients with incomplete resolution of inflammation during continuous therapy, which correlated with increased levels of TNF-α transcripts. Gut mucosal epithelial barrier disruption was evident by increased plasma bacterial 16S levels.
Loss of ANXA1 expression may support inflammation during IBD and can serve as a biomarker of disease progression. Changes in ANXA1 levels may be predictive of therapeutic efficacy.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24130820</pmid><doi>10.1371/journal.pone.0076969</doi><tpages>e76969</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-10, Vol.8 (10), p.e76969-e76969 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1441281057 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adult Aged Annexin A1 - blood Annexin A1 - genetics Annexin A1 - metabolism Annexins Anti-inflammatory agents Antibodies, Monoclonal - pharmacology Antibodies, Monoclonal - therapeutic use Arthritis Biochemistry Biological effects Biomarkers Biopsy Blood Crohn Disease - blood Crohn Disease - drug therapy Crohn Disease - immunology Crohn Disease - metabolism Crohn's disease Crohns disease Development and progression Disease Progression DNA, Bacterial - blood DNA, Ribosomal - blood Enzyme-linked immunosorbent assay Female Gastroenterology Gene expression Gene Expression Regulation Genetic factors Health aspects Hepatology Humans Immune response Immune system Immunology Immunomodulation Immunomodulators Inflammation Inflammation - genetics Inflammation - metabolism Inflammatory bowel disease Inflammatory bowel diseases Infliximab Intestinal Mucosa - drug effects Intestinal Mucosa - metabolism Intestine Laboratories Lymphocyte Activation - drug effects Male Middle Aged Monoclonal antibodies Mucosa Neutrophils Patients Peripheral blood mononuclear cells Proteins RNA, Messenger - genetics RNA, Messenger - metabolism Studies T-Lymphocytes - drug effects T-Lymphocytes - immunology Therapy Transcription Treatment Outcome Tumor necrosis factor Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-TNF Tumor necrosis factor-α Young Adult |
| title | Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease |
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