Experimental Immune-Mediated Pancreatitis in Neonatally Thymectomized Mice Immunized with Carbonic Anhydrase II and Lactoferrin
We previously reported that autoantibodies against carbonic anhydrase II and lactoferrin are frequently identified in patients with autoimmune-related pancreatitis. To clarify the role of carbonic anhydrase II and lactoferrin, we created animal models of autoimmune pancreatitis by immunizing neonata...
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| Veröffentlicht in: | Laboratory investigation 2002-04, Vol.82 (4), p.411-424 |
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| creator | Uchida, Kazushige Okazaki, Kazuichi Nishi, Toshiki Uose, Suguru Nakase, Hiroshi Ohana, Masaya Matsushima, Yumi Omori, Katsuyuki Chiba, Tsutomu |
| description | We previously reported that autoantibodies against carbonic anhydrase II and lactoferrin are frequently identified in patients with autoimmune-related pancreatitis. To clarify the role of carbonic anhydrase II and lactoferrin, we created animal models of autoimmune pancreatitis by immunizing neonatally thymectomized mice with carbonic anhydrase II and lactoferrin and also by transferring immunized spleen cells to nude mice. Neonatally thymectomized BALB/c mice were immunized with carbonic anhydrase II or lactoferrin followed by three booster injections (n = 10 in each group). We transferred whole, CD4+, or CD8+ spleen cells prepared from immunized neonatally thymectomized mice to nude mice (n = 5 in each group). Gene expression of IFN-γ and IL-4 was investigated using semiquantitative reverse transcription-polymerase chain reaction. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining was used to examine apoptosis. In immunized neonatally thymectomized mice, the prevalence of inflammation was significantly higher in the pancreas. Inflammation was present in all mice receiving whole or CD4+ cells. There was no change in any of the mice receiving CD8+ cells or nonimmunized spleen cells. Carbonic anhydrase II or lactoferrin-immunized mice had apoptotic duct cells or acinar cells, respectively. Expression of the IFN-γ gene was up-regulated in each group. Similar findings were observed in the salivary glands and liver. An immunologic mechanism against carbonic anhydrase II or lactoferrin is involved in the pathogenesis of these pancreatitis models, in which the effector cells are Th1-type CD4+ T cells. |
| doi_str_mv | 10.1038/labinvest.3780435 |
| format | Article |
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To clarify the role of carbonic anhydrase II and lactoferrin, we created animal models of autoimmune pancreatitis by immunizing neonatally thymectomized mice with carbonic anhydrase II and lactoferrin and also by transferring immunized spleen cells to nude mice. Neonatally thymectomized BALB/c mice were immunized with carbonic anhydrase II or lactoferrin followed by three booster injections (n = 10 in each group). We transferred whole, CD4+, or CD8+ spleen cells prepared from immunized neonatally thymectomized mice to nude mice (n = 5 in each group). Gene expression of IFN-γ and IL-4 was investigated using semiquantitative reverse transcription-polymerase chain reaction. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining was used to examine apoptosis. In immunized neonatally thymectomized mice, the prevalence of inflammation was significantly higher in the pancreas. Inflammation was present in all mice receiving whole or CD4+ cells. There was no change in any of the mice receiving CD8+ cells or nonimmunized spleen cells. Carbonic anhydrase II or lactoferrin-immunized mice had apoptotic duct cells or acinar cells, respectively. Expression of the IFN-γ gene was up-regulated in each group. Similar findings were observed in the salivary glands and liver. An immunologic mechanism against carbonic anhydrase II or lactoferrin is involved in the pathogenesis of these pancreatitis models, in which the effector cells are Th1-type CD4+ T cells.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.3780435</identifier><identifier>PMID: 11950899</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>Adoptive Transfer ; Animals ; Autoimmune Diseases - immunology ; Autoimmune Diseases - pathology ; Biological and medical sciences ; Carbonic Anhydrase II - administration & dosage ; Carbonic Anhydrase II - immunology ; CD4-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - immunology ; Disease Models, Animal ; Experimental and animal immunopathology. Animal models ; Female ; Gene Expression ; Immunization ; Immunopathology ; In Situ Nick-End Labeling ; Interferon-gamma - genetics ; Interferon-gamma - metabolism ; Interleukin-4 - genetics ; Interleukin-4 - metabolism ; Laboratory Medicine ; Lactoferrin - administration & dosage ; Lactoferrin - immunology ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Pancreas - immunology ; Pancreatitis - immunology ; Pancreatitis - pathology ; Pathology ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Salivary Glands - metabolism ; Spleen - immunology ; Thymectomy</subject><ispartof>Laboratory investigation, 2002-04, Vol.82 (4), p.411-424</ispartof><rights>2002 United States & Canadian Academy of Pathology</rights><rights>The United States and Canadian Academy of Pathology, Inc. 2002</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-42152a2091e62a7fda05085b809e62456ce921002139e85f87ea645e5a9f6283</citedby><cites>FETCH-LOGICAL-c524t-42152a2091e62a7fda05085b809e62456ce921002139e85f87ea645e5a9f6283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13609979$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11950899$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Uchida, Kazushige</creatorcontrib><creatorcontrib>Okazaki, Kazuichi</creatorcontrib><creatorcontrib>Nishi, Toshiki</creatorcontrib><creatorcontrib>Uose, Suguru</creatorcontrib><creatorcontrib>Nakase, Hiroshi</creatorcontrib><creatorcontrib>Ohana, Masaya</creatorcontrib><creatorcontrib>Matsushima, Yumi</creatorcontrib><creatorcontrib>Omori, Katsuyuki</creatorcontrib><creatorcontrib>Chiba, Tsutomu</creatorcontrib><title>Experimental Immune-Mediated Pancreatitis in Neonatally Thymectomized Mice Immunized with Carbonic Anhydrase II and Lactoferrin</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>We previously reported that autoantibodies against carbonic anhydrase II and lactoferrin are frequently identified in patients with autoimmune-related pancreatitis. To clarify the role of carbonic anhydrase II and lactoferrin, we created animal models of autoimmune pancreatitis by immunizing neonatally thymectomized mice with carbonic anhydrase II and lactoferrin and also by transferring immunized spleen cells to nude mice. Neonatally thymectomized BALB/c mice were immunized with carbonic anhydrase II or lactoferrin followed by three booster injections (n = 10 in each group). We transferred whole, CD4+, or CD8+ spleen cells prepared from immunized neonatally thymectomized mice to nude mice (n = 5 in each group). Gene expression of IFN-γ and IL-4 was investigated using semiquantitative reverse transcription-polymerase chain reaction. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining was used to examine apoptosis. In immunized neonatally thymectomized mice, the prevalence of inflammation was significantly higher in the pancreas. Inflammation was present in all mice receiving whole or CD4+ cells. There was no change in any of the mice receiving CD8+ cells or nonimmunized spleen cells. Carbonic anhydrase II or lactoferrin-immunized mice had apoptotic duct cells or acinar cells, respectively. Expression of the IFN-γ gene was up-regulated in each group. Similar findings were observed in the salivary glands and liver. An immunologic mechanism against carbonic anhydrase II or lactoferrin is involved in the pathogenesis of these pancreatitis models, in which the effector cells are Th1-type CD4+ T cells.</description><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - pathology</subject><subject>Biological and medical sciences</subject><subject>Carbonic Anhydrase II - administration & dosage</subject><subject>Carbonic Anhydrase II - immunology</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>Disease Models, Animal</subject><subject>Experimental and animal immunopathology. Animal models</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Immunization</subject><subject>Immunopathology</subject><subject>In Situ Nick-End Labeling</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-4 - genetics</subject><subject>Interleukin-4 - metabolism</subject><subject>Laboratory Medicine</subject><subject>Lactoferrin - administration & dosage</subject><subject>Lactoferrin - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Pancreas - immunology</subject><subject>Pancreatitis - immunology</subject><subject>Pancreatitis - pathology</subject><subject>Pathology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Salivary Glands - metabolism</subject><subject>Spleen - immunology</subject><subject>Thymectomy</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kk9v0zAYhy0EYt3gA3BBERLjlOE_sWNrp6kaUKkDDr1HrvOGekqcYieDcuGr845EVOLQk2X7-dl-38eEvGL0ilGh37d268MDpOFKlJoWQj4hCyYFzamg5VOyoJSLXGlRnpHzlO4pZUWh5HNyxpiRVBuzIL9vf-4h-g7CYNts1XVjgPwOam8HqLOvNrgIdvCDT5kP2Wfog0WwPWSb3aEDN_Sd_4XgnXcwpf9Of_hhly1t3PbBu-wm7A51tAmJVWZDna0tBhuI0YcX5Flj2wQv5_GCbD7cbpaf8vWXj6vlzTp3khdDXnAmueXUMFDclk1tKRYgt5oaXCikcmA4w3qZMKBlo0uwqpAgrWkU1-KCvJuO3cf--4gdqzqfHLStDdCPqSqlZIIbJZG8PE0yaQyXCsE3_4H3_RgDFlFxTrmWSjOE2AS52KcUoan22GwbDxWj1aPD6p_DanaImdfzweO2g_qYmKUh8HYGbHK2bSJa8unICUWNKR85PnEJt8I3iMcXnrr9egoB2njwGErOQ3D4JSL6ruren0j_AY2JzK4</recordid><startdate>20020401</startdate><enddate>20020401</enddate><creator>Uchida, Kazushige</creator><creator>Okazaki, Kazuichi</creator><creator>Nishi, Toshiki</creator><creator>Uose, Suguru</creator><creator>Nakase, Hiroshi</creator><creator>Ohana, Masaya</creator><creator>Matsushima, Yumi</creator><creator>Omori, Katsuyuki</creator><creator>Chiba, Tsutomu</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20020401</creationdate><title>Experimental Immune-Mediated Pancreatitis in Neonatally Thymectomized Mice Immunized with Carbonic Anhydrase II and Lactoferrin</title><author>Uchida, Kazushige ; Okazaki, Kazuichi ; Nishi, Toshiki ; Uose, Suguru ; Nakase, Hiroshi ; Ohana, Masaya ; Matsushima, Yumi ; Omori, Katsuyuki ; Chiba, Tsutomu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-42152a2091e62a7fda05085b809e62456ce921002139e85f87ea645e5a9f6283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>Autoimmune Diseases - immunology</topic><topic>Autoimmune Diseases - pathology</topic><topic>Biological and medical sciences</topic><topic>Carbonic Anhydrase II - administration & dosage</topic><topic>Carbonic Anhydrase II - immunology</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>Disease Models, Animal</topic><topic>Experimental and animal immunopathology. Animal models</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Immunization</topic><topic>Immunopathology</topic><topic>In Situ Nick-End Labeling</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-4 - genetics</topic><topic>Interleukin-4 - metabolism</topic><topic>Laboratory Medicine</topic><topic>Lactoferrin - administration & dosage</topic><topic>Lactoferrin - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Pancreas - immunology</topic><topic>Pancreatitis - immunology</topic><topic>Pancreatitis - pathology</topic><topic>Pathology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Salivary Glands - metabolism</topic><topic>Spleen - immunology</topic><topic>Thymectomy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Uchida, Kazushige</creatorcontrib><creatorcontrib>Okazaki, Kazuichi</creatorcontrib><creatorcontrib>Nishi, Toshiki</creatorcontrib><creatorcontrib>Uose, Suguru</creatorcontrib><creatorcontrib>Nakase, Hiroshi</creatorcontrib><creatorcontrib>Ohana, Masaya</creatorcontrib><creatorcontrib>Matsushima, Yumi</creatorcontrib><creatorcontrib>Omori, Katsuyuki</creatorcontrib><creatorcontrib>Chiba, Tsutomu</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech 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>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>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</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>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>MEDLINE - Academic</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Uchida, Kazushige</au><au>Okazaki, Kazuichi</au><au>Nishi, Toshiki</au><au>Uose, Suguru</au><au>Nakase, Hiroshi</au><au>Ohana, Masaya</au><au>Matsushima, Yumi</au><au>Omori, Katsuyuki</au><au>Chiba, Tsutomu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Experimental Immune-Mediated Pancreatitis in Neonatally Thymectomized Mice Immunized with Carbonic Anhydrase II and Lactoferrin</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2002-04-01</date><risdate>2002</risdate><volume>82</volume><issue>4</issue><spage>411</spage><epage>424</epage><pages>411-424</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><coden>LAINAW</coden><abstract>We previously reported that autoantibodies against carbonic anhydrase II and lactoferrin are frequently identified in patients with autoimmune-related pancreatitis. To clarify the role of carbonic anhydrase II and lactoferrin, we created animal models of autoimmune pancreatitis by immunizing neonatally thymectomized mice with carbonic anhydrase II and lactoferrin and also by transferring immunized spleen cells to nude mice. Neonatally thymectomized BALB/c mice were immunized with carbonic anhydrase II or lactoferrin followed by three booster injections (n = 10 in each group). We transferred whole, CD4+, or CD8+ spleen cells prepared from immunized neonatally thymectomized mice to nude mice (n = 5 in each group). Gene expression of IFN-γ and IL-4 was investigated using semiquantitative reverse transcription-polymerase chain reaction. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining was used to examine apoptosis. In immunized neonatally thymectomized mice, the prevalence of inflammation was significantly higher in the pancreas. Inflammation was present in all mice receiving whole or CD4+ cells. There was no change in any of the mice receiving CD8+ cells or nonimmunized spleen cells. Carbonic anhydrase II or lactoferrin-immunized mice had apoptotic duct cells or acinar cells, respectively. Expression of the IFN-γ gene was up-regulated in each group. Similar findings were observed in the salivary glands and liver. An immunologic mechanism against carbonic anhydrase II or lactoferrin is involved in the pathogenesis of these pancreatitis models, in which the effector cells are Th1-type CD4+ T cells.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>11950899</pmid><doi>10.1038/labinvest.3780435</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Laboratory investigation, 2002-04, Vol.82 (4), p.411-424 |
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| subjects | Adoptive Transfer Animals Autoimmune Diseases - immunology Autoimmune Diseases - pathology Biological and medical sciences Carbonic Anhydrase II - administration & dosage Carbonic Anhydrase II - immunology CD4-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - immunology Disease Models, Animal Experimental and animal immunopathology. Animal models Female Gene Expression Immunization Immunopathology In Situ Nick-End Labeling Interferon-gamma - genetics Interferon-gamma - metabolism Interleukin-4 - genetics Interleukin-4 - metabolism Laboratory Medicine Lactoferrin - administration & dosage Lactoferrin - immunology Male Medical sciences Medicine Medicine & Public Health Mice Mice, Inbred BALB C Mice, Nude Pancreas - immunology Pancreatitis - immunology Pancreatitis - pathology Pathology Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Salivary Glands - metabolism Spleen - immunology Thymectomy |
| title | Experimental Immune-Mediated Pancreatitis in Neonatally Thymectomized Mice Immunized with Carbonic Anhydrase II and Lactoferrin |
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