Borrelia burgdorferi NapA–driven Th17 cell inflammation in lyme arthritis
Objective Human Lyme arthritis caused by Borrelia burgdorferi is characterized by an inflammatory infiltrate that consists mainly of neutrophils and T cells. This study was undertaken to evaluate the role of the innate and acquired immune responses elicited by the neutrophil‐activating protein A (Na...
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| Veröffentlicht in: | Arthritis and rheumatism 2008-11, Vol.58 (11), p.3609-3617 |
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| creator | Codolo, Gaia Amedei, Amedeo Steere, Allen C. Papinutto, Elena Cappon, Andrea Polenghi, Alessandra Benagiano, Marisa Paccani, Silvia Rossi Sambri, Vittorio Del Prete, Gianfranco Baldari, Cosima Tatiana Zanotti, Giuseppe Montecucco, Cesare D'Elios, Mario Milco de Bernard, Marina |
| description | Objective
Human Lyme arthritis caused by Borrelia burgdorferi is characterized by an inflammatory infiltrate that consists mainly of neutrophils and T cells. This study was undertaken to evaluate the role of the innate and acquired immune responses elicited by the neutrophil‐activating protein A (NapA) of B burgdorferi in patients with Lyme arthritis.
Methods
Serum anti‐NapA antibodies were measured in 27 patients with Lyme arthritis and 30 healthy control subjects. The cytokine profile of synovial fluid T cells specific for NapA was investigated in 5 patients with Lyme arthritis. The cytokine profile induced by NapA in neutrophils and monocytes was also investigated.
Results
Serum anti‐NapA antibodies were found in 48% of the patients with Lyme arthritis but were undetectable in the healthy controls. T cells from the synovial fluid of patients with Lyme arthritis produced interleukin‐17 (IL‐17) in response to NapA. Moreover, NapA was able to induce the expression of IL‐23 in neutrophils and monocytes, as well as the expression of IL‐6, IL‐1β, and transforming growth factor β (TGFβ) in monocytes, via Toll‐like receptor 2.
Conclusion
These findings indicate that NapA of B burgdorferi is able to drive the expression of IL‐6, IL‐1β, IL‐23, and TGFβ by cells of the innate immune system and to elicit a synovial fluid Th17 cell response that might play a crucial role in the pathogenesis of Lyme arthritis. |
| doi_str_mv | 10.1002/art.23972 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69771247</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69771247</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3892-2c97da3aa1725f438b78b3cffedac5fa7efeb192d82c1d50d7678aaed62fa03b3</originalsourceid><addsrcrecordid>eNp1kMtKAzEUhoMotlYXvoDMSnAxbS4zzWRZizcsClLX4cwksZG51GRG6c538A19ElOn4MrV4YeP7_z8CJ0SPCYY0wm4dkyZ4HQPDUlKRYwJI_toiDFOYpYKMkBH3r-GSFnKDtGAZIKnLGFDdH_ZOKdLC1HeuRfVOKOdjR5gPfv-_FLOvus6Wq4IjwpdlpGtTQlVBa1t6hCiclPpKHxfOdtaf4wODJRen-zuCD1fXy3nt_Hi8eZuPlvEBcsEjWkhuAIGQDhNTcKynGc5K4zRCorUANdG50RQldGCqBQrPuUZgFZTagCznI3Qee9du-at076VlfXbflDrpvNyKjgnNOEBvOjBwjXeO23k2tkK3EYSLLfLydBd_i4X2LOdtMsrrf7I3VQBmPTAhy315n-TnD0te-UPvON58g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69771247</pqid></control><display><type>article</type><title>Borrelia burgdorferi NapA–driven Th17 cell inflammation in lyme arthritis</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Codolo, Gaia ; Amedei, Amedeo ; Steere, Allen C. ; Papinutto, Elena ; Cappon, Andrea ; Polenghi, Alessandra ; Benagiano, Marisa ; Paccani, Silvia Rossi ; Sambri, Vittorio ; Del Prete, Gianfranco ; Baldari, Cosima Tatiana ; Zanotti, Giuseppe ; Montecucco, Cesare ; D'Elios, Mario Milco ; de Bernard, Marina</creator><creatorcontrib>Codolo, Gaia ; Amedei, Amedeo ; Steere, Allen C. ; Papinutto, Elena ; Cappon, Andrea ; Polenghi, Alessandra ; Benagiano, Marisa ; Paccani, Silvia Rossi ; Sambri, Vittorio ; Del Prete, Gianfranco ; Baldari, Cosima Tatiana ; Zanotti, Giuseppe ; Montecucco, Cesare ; D'Elios, Mario Milco ; de Bernard, Marina</creatorcontrib><description>Objective
Human Lyme arthritis caused by Borrelia burgdorferi is characterized by an inflammatory infiltrate that consists mainly of neutrophils and T cells. This study was undertaken to evaluate the role of the innate and acquired immune responses elicited by the neutrophil‐activating protein A (NapA) of B burgdorferi in patients with Lyme arthritis.
Methods
Serum anti‐NapA antibodies were measured in 27 patients with Lyme arthritis and 30 healthy control subjects. The cytokine profile of synovial fluid T cells specific for NapA was investigated in 5 patients with Lyme arthritis. The cytokine profile induced by NapA in neutrophils and monocytes was also investigated.
Results
Serum anti‐NapA antibodies were found in 48% of the patients with Lyme arthritis but were undetectable in the healthy controls. T cells from the synovial fluid of patients with Lyme arthritis produced interleukin‐17 (IL‐17) in response to NapA. Moreover, NapA was able to induce the expression of IL‐23 in neutrophils and monocytes, as well as the expression of IL‐6, IL‐1β, and transforming growth factor β (TGFβ) in monocytes, via Toll‐like receptor 2.
Conclusion
These findings indicate that NapA of B burgdorferi is able to drive the expression of IL‐6, IL‐1β, IL‐23, and TGFβ by cells of the innate immune system and to elicit a synovial fluid Th17 cell response that might play a crucial role in the pathogenesis of Lyme arthritis.</description><identifier>ISSN: 0004-3591</identifier><identifier>EISSN: 1529-0131</identifier><identifier>DOI: 10.1002/art.23972</identifier><identifier>PMID: 18975343</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adolescent ; Adult ; Antibodies, Bacterial - analysis ; Bacterial Proteins - immunology ; Borrelia burgdorferi - immunology ; Chemokines, CXC - immunology ; Child ; Female ; Humans ; Interleukin-17 - biosynthesis ; Interleukin-17 - immunology ; Interleukin-1beta - biosynthesis ; Interleukin-23 - biosynthesis ; Interleukin-6 - biosynthesis ; Lyme Disease - immunology ; Male ; Middle Aged ; Monocytes - immunology ; Neutrophils - immunology ; Synovial Fluid - immunology ; T-Lymphocytes - immunology ; Transforming Growth Factor beta - biosynthesis</subject><ispartof>Arthritis and rheumatism, 2008-11, Vol.58 (11), p.3609-3617</ispartof><rights>Copyright © 2008 by the American College of Rheumatology</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3892-2c97da3aa1725f438b78b3cffedac5fa7efeb192d82c1d50d7678aaed62fa03b3</citedby><cites>FETCH-LOGICAL-c3892-2c97da3aa1725f438b78b3cffedac5fa7efeb192d82c1d50d7678aaed62fa03b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fart.23972$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.23972$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,27931,27932,45581,45582</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18975343$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Codolo, Gaia</creatorcontrib><creatorcontrib>Amedei, Amedeo</creatorcontrib><creatorcontrib>Steere, Allen C.</creatorcontrib><creatorcontrib>Papinutto, Elena</creatorcontrib><creatorcontrib>Cappon, Andrea</creatorcontrib><creatorcontrib>Polenghi, Alessandra</creatorcontrib><creatorcontrib>Benagiano, Marisa</creatorcontrib><creatorcontrib>Paccani, Silvia Rossi</creatorcontrib><creatorcontrib>Sambri, Vittorio</creatorcontrib><creatorcontrib>Del Prete, Gianfranco</creatorcontrib><creatorcontrib>Baldari, Cosima Tatiana</creatorcontrib><creatorcontrib>Zanotti, Giuseppe</creatorcontrib><creatorcontrib>Montecucco, Cesare</creatorcontrib><creatorcontrib>D'Elios, Mario Milco</creatorcontrib><creatorcontrib>de Bernard, Marina</creatorcontrib><title>Borrelia burgdorferi NapA–driven Th17 cell inflammation in lyme arthritis</title><title>Arthritis and rheumatism</title><addtitle>Arthritis Rheum</addtitle><description>Objective
Human Lyme arthritis caused by Borrelia burgdorferi is characterized by an inflammatory infiltrate that consists mainly of neutrophils and T cells. This study was undertaken to evaluate the role of the innate and acquired immune responses elicited by the neutrophil‐activating protein A (NapA) of B burgdorferi in patients with Lyme arthritis.
Methods
Serum anti‐NapA antibodies were measured in 27 patients with Lyme arthritis and 30 healthy control subjects. The cytokine profile of synovial fluid T cells specific for NapA was investigated in 5 patients with Lyme arthritis. The cytokine profile induced by NapA in neutrophils and monocytes was also investigated.
Results
Serum anti‐NapA antibodies were found in 48% of the patients with Lyme arthritis but were undetectable in the healthy controls. T cells from the synovial fluid of patients with Lyme arthritis produced interleukin‐17 (IL‐17) in response to NapA. Moreover, NapA was able to induce the expression of IL‐23 in neutrophils and monocytes, as well as the expression of IL‐6, IL‐1β, and transforming growth factor β (TGFβ) in monocytes, via Toll‐like receptor 2.
Conclusion
These findings indicate that NapA of B burgdorferi is able to drive the expression of IL‐6, IL‐1β, IL‐23, and TGFβ by cells of the innate immune system and to elicit a synovial fluid Th17 cell response that might play a crucial role in the pathogenesis of Lyme arthritis.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Antibodies, Bacterial - analysis</subject><subject>Bacterial Proteins - immunology</subject><subject>Borrelia burgdorferi - immunology</subject><subject>Chemokines, CXC - immunology</subject><subject>Child</subject><subject>Female</subject><subject>Humans</subject><subject>Interleukin-17 - biosynthesis</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-1beta - biosynthesis</subject><subject>Interleukin-23 - biosynthesis</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Lyme Disease - immunology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Monocytes - immunology</subject><subject>Neutrophils - immunology</subject><subject>Synovial Fluid - immunology</subject><subject>T-Lymphocytes - immunology</subject><subject>Transforming Growth Factor beta - biosynthesis</subject><issn>0004-3591</issn><issn>1529-0131</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtKAzEUhoMotlYXvoDMSnAxbS4zzWRZizcsClLX4cwksZG51GRG6c538A19ElOn4MrV4YeP7_z8CJ0SPCYY0wm4dkyZ4HQPDUlKRYwJI_toiDFOYpYKMkBH3r-GSFnKDtGAZIKnLGFDdH_ZOKdLC1HeuRfVOKOdjR5gPfv-_FLOvus6Wq4IjwpdlpGtTQlVBa1t6hCiclPpKHxfOdtaf4wODJRen-zuCD1fXy3nt_Hi8eZuPlvEBcsEjWkhuAIGQDhNTcKynGc5K4zRCorUANdG50RQldGCqBQrPuUZgFZTagCznI3Qee9du-at076VlfXbflDrpvNyKjgnNOEBvOjBwjXeO23k2tkK3EYSLLfLydBd_i4X2LOdtMsrrf7I3VQBmPTAhy315n-TnD0te-UPvON58g</recordid><startdate>200811</startdate><enddate>200811</enddate><creator>Codolo, Gaia</creator><creator>Amedei, Amedeo</creator><creator>Steere, Allen C.</creator><creator>Papinutto, Elena</creator><creator>Cappon, Andrea</creator><creator>Polenghi, Alessandra</creator><creator>Benagiano, Marisa</creator><creator>Paccani, Silvia Rossi</creator><creator>Sambri, Vittorio</creator><creator>Del Prete, Gianfranco</creator><creator>Baldari, Cosima Tatiana</creator><creator>Zanotti, Giuseppe</creator><creator>Montecucco, Cesare</creator><creator>D'Elios, Mario Milco</creator><creator>de Bernard, Marina</creator><general>Wiley Subscription Services, Inc., A Wiley Company</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></search><sort><creationdate>200811</creationdate><title>Borrelia burgdorferi NapA–driven Th17 cell inflammation in lyme arthritis</title><author>Codolo, Gaia ; Amedei, Amedeo ; Steere, Allen C. ; Papinutto, Elena ; Cappon, Andrea ; Polenghi, Alessandra ; Benagiano, Marisa ; Paccani, Silvia Rossi ; Sambri, Vittorio ; Del Prete, Gianfranco ; Baldari, Cosima Tatiana ; Zanotti, Giuseppe ; Montecucco, Cesare ; D'Elios, Mario Milco ; de Bernard, Marina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3892-2c97da3aa1725f438b78b3cffedac5fa7efeb192d82c1d50d7678aaed62fa03b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Antibodies, Bacterial - analysis</topic><topic>Bacterial Proteins - immunology</topic><topic>Borrelia burgdorferi - immunology</topic><topic>Chemokines, CXC - immunology</topic><topic>Child</topic><topic>Female</topic><topic>Humans</topic><topic>Interleukin-17 - biosynthesis</topic><topic>Interleukin-17 - immunology</topic><topic>Interleukin-1beta - biosynthesis</topic><topic>Interleukin-23 - biosynthesis</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Lyme Disease - immunology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Monocytes - immunology</topic><topic>Neutrophils - immunology</topic><topic>Synovial Fluid - immunology</topic><topic>T-Lymphocytes - immunology</topic><topic>Transforming Growth Factor beta - biosynthesis</topic><toplevel>online_resources</toplevel><creatorcontrib>Codolo, Gaia</creatorcontrib><creatorcontrib>Amedei, Amedeo</creatorcontrib><creatorcontrib>Steere, Allen C.</creatorcontrib><creatorcontrib>Papinutto, Elena</creatorcontrib><creatorcontrib>Cappon, Andrea</creatorcontrib><creatorcontrib>Polenghi, Alessandra</creatorcontrib><creatorcontrib>Benagiano, Marisa</creatorcontrib><creatorcontrib>Paccani, Silvia Rossi</creatorcontrib><creatorcontrib>Sambri, Vittorio</creatorcontrib><creatorcontrib>Del Prete, Gianfranco</creatorcontrib><creatorcontrib>Baldari, Cosima Tatiana</creatorcontrib><creatorcontrib>Zanotti, Giuseppe</creatorcontrib><creatorcontrib>Montecucco, Cesare</creatorcontrib><creatorcontrib>D'Elios, Mario Milco</creatorcontrib><creatorcontrib>de Bernard, Marina</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Arthritis and rheumatism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Codolo, Gaia</au><au>Amedei, Amedeo</au><au>Steere, Allen C.</au><au>Papinutto, Elena</au><au>Cappon, Andrea</au><au>Polenghi, Alessandra</au><au>Benagiano, Marisa</au><au>Paccani, Silvia Rossi</au><au>Sambri, Vittorio</au><au>Del Prete, Gianfranco</au><au>Baldari, Cosima Tatiana</au><au>Zanotti, Giuseppe</au><au>Montecucco, Cesare</au><au>D'Elios, Mario Milco</au><au>de Bernard, Marina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Borrelia burgdorferi NapA–driven Th17 cell inflammation in lyme arthritis</atitle><jtitle>Arthritis and rheumatism</jtitle><addtitle>Arthritis Rheum</addtitle><date>2008-11</date><risdate>2008</risdate><volume>58</volume><issue>11</issue><spage>3609</spage><epage>3617</epage><pages>3609-3617</pages><issn>0004-3591</issn><eissn>1529-0131</eissn><abstract>Objective
Human Lyme arthritis caused by Borrelia burgdorferi is characterized by an inflammatory infiltrate that consists mainly of neutrophils and T cells. This study was undertaken to evaluate the role of the innate and acquired immune responses elicited by the neutrophil‐activating protein A (NapA) of B burgdorferi in patients with Lyme arthritis.
Methods
Serum anti‐NapA antibodies were measured in 27 patients with Lyme arthritis and 30 healthy control subjects. The cytokine profile of synovial fluid T cells specific for NapA was investigated in 5 patients with Lyme arthritis. The cytokine profile induced by NapA in neutrophils and monocytes was also investigated.
Results
Serum anti‐NapA antibodies were found in 48% of the patients with Lyme arthritis but were undetectable in the healthy controls. T cells from the synovial fluid of patients with Lyme arthritis produced interleukin‐17 (IL‐17) in response to NapA. Moreover, NapA was able to induce the expression of IL‐23 in neutrophils and monocytes, as well as the expression of IL‐6, IL‐1β, and transforming growth factor β (TGFβ) in monocytes, via Toll‐like receptor 2.
Conclusion
These findings indicate that NapA of B burgdorferi is able to drive the expression of IL‐6, IL‐1β, IL‐23, and TGFβ by cells of the innate immune system and to elicit a synovial fluid Th17 cell response that might play a crucial role in the pathogenesis of Lyme arthritis.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>18975343</pmid><doi>10.1002/art.23972</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Antibodies, Bacterial - analysis Bacterial Proteins - immunology Borrelia burgdorferi - immunology Chemokines, CXC - immunology Child Female Humans Interleukin-17 - biosynthesis Interleukin-17 - immunology Interleukin-1beta - biosynthesis Interleukin-23 - biosynthesis Interleukin-6 - biosynthesis Lyme Disease - immunology Male Middle Aged Monocytes - immunology Neutrophils - immunology Synovial Fluid - immunology T-Lymphocytes - immunology Transforming Growth Factor beta - biosynthesis |
| title | Borrelia burgdorferi NapA–driven Th17 cell inflammation in lyme arthritis |
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