Mycobacteria-induced anaemia revisited: A molecular approach reveals the involvement of NRAMP1 and lipocalin-2, but not of hepcidin
Abstract Anaemia is a frequent complication of chronic infectious diseases but the exact mechanisms by which it develops remain to be clarified. In the present work, we used a mouse model of mycobacterial infection to study molecular alterations of iron metabolism induced by infection. We show that...
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| Veröffentlicht in: | Immunobiology (1979) 2011-10, Vol.216 (10), p.1127-1134 |
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| creator | Rodrigues, Pedro N Gomes, Sandro S Neves, João V Gomes-Pereira, Sandra Correia-Neves, Margarida Nunes-Alves, Cláudio Stolte, Jens Sanchez, Mayka Appelberg, Rui Muckenthaler, Martina U Gomes, M. Salomé |
| description | Abstract Anaemia is a frequent complication of chronic infectious diseases but the exact mechanisms by which it develops remain to be clarified. In the present work, we used a mouse model of mycobacterial infection to study molecular alterations of iron metabolism induced by infection. We show that four weeks after infection with Mycobacterium avium BALB/c mice exhibited a moderate anaemia, which was not accompanied by an increase on hepatic hepcidin mRNA expression. Instead, infected mice presented increased mRNA expression of ferroportin ( Slc40a1 ), ceruloplasmin ( Cp ), hemopexin ( Hpx ), heme-oxygenase-1 ( Hmox1 ) and lipocalin-2 ( Lcn2 ). Both the anaemia and the mRNA expression changes of iron-related genes were largely absent in C.D2 mice which bear a functional allele of the Nramp1 gene. Data presented in this work suggest that anaemia due to a chronic mycobacterial infection may develop in the absence of elevated hepcidin expression, is influenced by Nramp1 and may involve lipocalin-2. |
| doi_str_mv | 10.1016/j.imbio.2011.04.004 |
| format | Article |
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Salomé</creator><creatorcontrib>Rodrigues, Pedro N ; Gomes, Sandro S ; Neves, João V ; Gomes-Pereira, Sandra ; Correia-Neves, Margarida ; Nunes-Alves, Cláudio ; Stolte, Jens ; Sanchez, Mayka ; Appelberg, Rui ; Muckenthaler, Martina U ; Gomes, M. Salomé</creatorcontrib><description>Abstract Anaemia is a frequent complication of chronic infectious diseases but the exact mechanisms by which it develops remain to be clarified. In the present work, we used a mouse model of mycobacterial infection to study molecular alterations of iron metabolism induced by infection. We show that four weeks after infection with Mycobacterium avium BALB/c mice exhibited a moderate anaemia, which was not accompanied by an increase on hepatic hepcidin mRNA expression. Instead, infected mice presented increased mRNA expression of ferroportin ( Slc40a1 ), ceruloplasmin ( Cp ), hemopexin ( Hpx ), heme-oxygenase-1 ( Hmox1 ) and lipocalin-2 ( Lcn2 ). Both the anaemia and the mRNA expression changes of iron-related genes were largely absent in C.D2 mice which bear a functional allele of the Nramp1 gene. Data presented in this work suggest that anaemia due to a chronic mycobacterial infection may develop in the absence of elevated hepcidin expression, is influenced by Nramp1 and may involve lipocalin-2.</description><identifier>ISSN: 0171-2985</identifier><identifier>EISSN: 1878-3279</identifier><identifier>DOI: 10.1016/j.imbio.2011.04.004</identifier><identifier>PMID: 21601942</identifier><language>eng</language><publisher>Netherlands: Elsevier GmbH</publisher><subject>Advanced Basic Science ; Allergy and Immunology ; Anaemia ; Anemia - metabolism ; Anemia - microbiology ; Anemia - pathology ; Animals ; Antimicrobial Cationic Peptides - genetics ; Antimicrobial Cationic Peptides - metabolism ; Cation Transport Proteins - genetics ; Cation Transport Proteins - metabolism ; Disease Models, Animal ; Gene Expression Profiling ; Gene Expression Regulation ; Hepcidin ; Hepcidins ; Iron - metabolism ; Lipocalin-2 ; Lipocalins - genetics ; Lipocalins - metabolism ; Liver - metabolism ; Liver - pathology ; Metabolic Networks and Pathways - genetics ; Mice ; Mice, Inbred BALB C ; Mycobacteria ; Mycobacterium avium ; Mycobacterium avium - physiology ; NRAMP1 ; RNA, Messenger - genetics ; Tuberculosis - metabolism ; Tuberculosis - microbiology ; Tuberculosis - pathology</subject><ispartof>Immunobiology (1979), 2011-10, Vol.216 (10), p.1127-1134</ispartof><rights>Elsevier GmbH</rights><rights>2011 Elsevier GmbH</rights><rights>Copyright © 2011 Elsevier GmbH. 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Salomé</creatorcontrib><title>Mycobacteria-induced anaemia revisited: A molecular approach reveals the involvement of NRAMP1 and lipocalin-2, but not of hepcidin</title><title>Immunobiology (1979)</title><addtitle>Immunobiology</addtitle><description>Abstract Anaemia is a frequent complication of chronic infectious diseases but the exact mechanisms by which it develops remain to be clarified. In the present work, we used a mouse model of mycobacterial infection to study molecular alterations of iron metabolism induced by infection. We show that four weeks after infection with Mycobacterium avium BALB/c mice exhibited a moderate anaemia, which was not accompanied by an increase on hepatic hepcidin mRNA expression. Instead, infected mice presented increased mRNA expression of ferroportin ( Slc40a1 ), ceruloplasmin ( Cp ), hemopexin ( Hpx ), heme-oxygenase-1 ( Hmox1 ) and lipocalin-2 ( Lcn2 ). Both the anaemia and the mRNA expression changes of iron-related genes were largely absent in C.D2 mice which bear a functional allele of the Nramp1 gene. Data presented in this work suggest that anaemia due to a chronic mycobacterial infection may develop in the absence of elevated hepcidin expression, is influenced by Nramp1 and may involve lipocalin-2.</description><subject>Advanced Basic Science</subject><subject>Allergy and Immunology</subject><subject>Anaemia</subject><subject>Anemia - metabolism</subject><subject>Anemia - microbiology</subject><subject>Anemia - pathology</subject><subject>Animals</subject><subject>Antimicrobial Cationic Peptides - genetics</subject><subject>Antimicrobial Cationic Peptides - metabolism</subject><subject>Cation Transport Proteins - genetics</subject><subject>Cation Transport Proteins - metabolism</subject><subject>Disease Models, Animal</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Hepcidin</subject><subject>Hepcidins</subject><subject>Iron - metabolism</subject><subject>Lipocalin-2</subject><subject>Lipocalins - genetics</subject><subject>Lipocalins - metabolism</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Metabolic Networks and Pathways - genetics</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mycobacteria</subject><subject>Mycobacterium avium</subject><subject>Mycobacterium avium - physiology</subject><subject>NRAMP1</subject><subject>RNA, Messenger - genetics</subject><subject>Tuberculosis - metabolism</subject><subject>Tuberculosis - microbiology</subject><subject>Tuberculosis - pathology</subject><issn>0171-2985</issn><issn>1878-3279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkkuLFDEUhQtRnHb0FwiSnRurvDf1SgSFZtAZYUbFxzqkklt02qpKm1Q19No_bnp6dOFmVgnknJPL-W6WPUcoELB5vS3c2DlfcEAsoCoAqgfZCkUr8pK38mG2Amwx51LUZ9mTGLcAKHkrHmdnHJt0r_gq-31zML7TZqbgdO4muxiyTE-aRqdZoL2Lbib7hq3Z6Acyy6AD07td8Npsju-kh8jmDTE37f2wp5Gmmfmeffq6vvmCKcmywe280YObcv6KdcvMJn8r2dDOOOump9mjPqXQs7vzPPvx4f33i6v8-vPlx4v1dW5qbOaca-hFrXnfW1FyoJ6TqG3ZSAtoTF82hjdCtGgFdY1AXXFJ0EHdQd80WtblefbylJum_7VQnNXooqFh0BP5JSoJVSWbsm3vVQpRS5AtyqQsT0oTfIyBerULbtThoBDUEZPaqltM6ohJQaUSpuR6cZe_dCPZf56_XJLg7UlAqY-9o6CicTQlNi6QmZX17p4P3v3nN6l_lyj8pAPFrV_ClKpWqCJXoL4dN-W4KIgA0NZY_gGctLnB</recordid><startdate>20111001</startdate><enddate>20111001</enddate><creator>Rodrigues, Pedro N</creator><creator>Gomes, Sandro S</creator><creator>Neves, João V</creator><creator>Gomes-Pereira, Sandra</creator><creator>Correia-Neves, Margarida</creator><creator>Nunes-Alves, Cláudio</creator><creator>Stolte, Jens</creator><creator>Sanchez, Mayka</creator><creator>Appelberg, Rui</creator><creator>Muckenthaler, Martina U</creator><creator>Gomes, M. Salomé</creator><general>Elsevier GmbH</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>7X8</scope><scope>7QL</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>20111001</creationdate><title>Mycobacteria-induced anaemia revisited: A molecular approach reveals the involvement of NRAMP1 and lipocalin-2, but not of hepcidin</title><author>Rodrigues, Pedro N ; Gomes, Sandro S ; Neves, João V ; Gomes-Pereira, Sandra ; Correia-Neves, Margarida ; Nunes-Alves, Cláudio ; Stolte, Jens ; Sanchez, Mayka ; Appelberg, Rui ; Muckenthaler, Martina U ; Gomes, M. 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| subjects | Advanced Basic Science Allergy and Immunology Anaemia Anemia - metabolism Anemia - microbiology Anemia - pathology Animals Antimicrobial Cationic Peptides - genetics Antimicrobial Cationic Peptides - metabolism Cation Transport Proteins - genetics Cation Transport Proteins - metabolism Disease Models, Animal Gene Expression Profiling Gene Expression Regulation Hepcidin Hepcidins Iron - metabolism Lipocalin-2 Lipocalins - genetics Lipocalins - metabolism Liver - metabolism Liver - pathology Metabolic Networks and Pathways - genetics Mice Mice, Inbred BALB C Mycobacteria Mycobacterium avium Mycobacterium avium - physiology NRAMP1 RNA, Messenger - genetics Tuberculosis - metabolism Tuberculosis - microbiology Tuberculosis - pathology |
| title | Mycobacteria-induced anaemia revisited: A molecular approach reveals the involvement of NRAMP1 and lipocalin-2, but not of hepcidin |
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