Chlamydophila pneumoniae phospholipase D (CpPLD) drives Th17 inflammation in human atherosclerosis

Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential to interfere with cellular signaling cascades and to modulate the host-immune response. Here, we investigated the role of the innate and acqui...

Full description

Saved in:

Bibliographic Details
Published in:	Proceedings of the National Academy of Sciences - PNAS Vol. 109; no. 4; p. 1222
Main Authors:	Benagiano, Marisa, Munari, Fabio, Ciervo, Alessandra, Amedei, Amedeo, Paccani, Silvia Rossi, Mancini, Fabiola, Ferrari, Mauro, Della Bella, Chiara, Ulivi, Camilla, D'Elios, Sofia, Baldari, Cosima T, Prisco, Domenico, de Bernard, Marina, D'Elios, Mario M
Format:	Journal Article
Language:	English
Published:	United States 24.01.2012
Subjects:	Aged Atherosclerosis - immunology Atherosclerosis - microbiology Cell Line Chemokines - immunology Chlamydophila pneumoniae - enzymology Cytokines - immunology Enzyme-Linked Immunosorbent Assay Female Gene Expression Regulation - immunology Human Umbilical Vein Endothelial Cells Humans Male Matrix Metalloproteinase 9 - metabolism Middle Aged Monocytes - immunology Phospholipase D - immunology Phospholipase D - pharmacology Real-Time Polymerase Chain Reaction Th17 Cells - immunology Thromboplastin - metabolism Toll-Like Receptor 4 - agonists
ISSN:	1091-6490, 1091-6490
Online Access:	Get more information
Tags:	Add Tag No Tags, Be the first to tag this record!

Abstract	Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential to interfere with cellular signaling cascades and to modulate the host-immune response. Here, we investigated the role of the innate and acquired immune responses elicited by Chlamydophila pneumoniae phospholipase D (CpPLD) in the pathogenesis of atherosclerosis. We evaluated the cytokine and chemokine production induced by CpPLD in healthy donors' monocytes and in vivo activated T cells specific for CpPLD that infiltrate atherosclerotic lesions of patients with C. pneumoniae antibodies. We also examined the helper function of CpPLD-specific T cells for monocyte matrix metalloproteinase (MMP)-9 and tissue factor (TF) production as well as the CpPLD-induced chemokine expression by human venular endothelial cells (HUVECs). We report here that CpPLD is a TLR4 agonist able to induce the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 in monocytes, as well as CXCL-9, CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs. Plaque-derived T cells produce IL-17 in response to CpPLD. Moreover, CpPLD-specific CD4(+) T lymphocytes display helper function for monocyte MMP-9 and TF production. CpPLD promotes Th17 cell migration through the induction of chemokine secretion and adhesion molecule expression on endothelial cells. These findings indicate that CpPLD is able to drive the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 by monocytes and to elicit a Th17 immune response that plays a key role in the genesis of atherosclerosis.
AbstractList	Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential to interfere with cellular signaling cascades and to modulate the host-immune response. Here, we investigated the role of the innate and acquired immune responses elicited by Chlamydophila pneumoniae phospholipase D (CpPLD) in the pathogenesis of atherosclerosis. We evaluated the cytokine and chemokine production induced by CpPLD in healthy donors' monocytes and in vivo activated T cells specific for CpPLD that infiltrate atherosclerotic lesions of patients with C. pneumoniae antibodies. We also examined the helper function of CpPLD-specific T cells for monocyte matrix metalloproteinase (MMP)-9 and tissue factor (TF) production as well as the CpPLD-induced chemokine expression by human venular endothelial cells (HUVECs). We report here that CpPLD is a TLR4 agonist able to induce the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 in monocytes, as well as CXCL-9, CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs. Plaque-derived T cells produce IL-17 in response to CpPLD. Moreover, CpPLD-specific CD4(+) T lymphocytes display helper function for monocyte MMP-9 and TF production. CpPLD promotes Th17 cell migration through the induction of chemokine secretion and adhesion molecule expression on endothelial cells. These findings indicate that CpPLD is able to drive the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 by monocytes and to elicit a Th17 immune response that plays a key role in the genesis of atherosclerosis.Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential to interfere with cellular signaling cascades and to modulate the host-immune response. Here, we investigated the role of the innate and acquired immune responses elicited by Chlamydophila pneumoniae phospholipase D (CpPLD) in the pathogenesis of atherosclerosis. We evaluated the cytokine and chemokine production induced by CpPLD in healthy donors' monocytes and in vivo activated T cells specific for CpPLD that infiltrate atherosclerotic lesions of patients with C. pneumoniae antibodies. We also examined the helper function of CpPLD-specific T cells for monocyte matrix metalloproteinase (MMP)-9 and tissue factor (TF) production as well as the CpPLD-induced chemokine expression by human venular endothelial cells (HUVECs). We report here that CpPLD is a TLR4 agonist able to induce the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 in monocytes, as well as CXCL-9, CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs. Plaque-derived T cells produce IL-17 in response to CpPLD. Moreover, CpPLD-specific CD4(+) T lymphocytes display helper function for monocyte MMP-9 and TF production. CpPLD promotes Th17 cell migration through the induction of chemokine secretion and adhesion molecule expression on endothelial cells. These findings indicate that CpPLD is able to drive the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 by monocytes and to elicit a Th17 immune response that plays a key role in the genesis of atherosclerosis. Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential to interfere with cellular signaling cascades and to modulate the host-immune response. Here, we investigated the role of the innate and acquired immune responses elicited by Chlamydophila pneumoniae phospholipase D (CpPLD) in the pathogenesis of atherosclerosis. We evaluated the cytokine and chemokine production induced by CpPLD in healthy donors' monocytes and in vivo activated T cells specific for CpPLD that infiltrate atherosclerotic lesions of patients with C. pneumoniae antibodies. We also examined the helper function of CpPLD-specific T cells for monocyte matrix metalloproteinase (MMP)-9 and tissue factor (TF) production as well as the CpPLD-induced chemokine expression by human venular endothelial cells (HUVECs). We report here that CpPLD is a TLR4 agonist able to induce the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 in monocytes, as well as CXCL-9, CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs. Plaque-derived T cells produce IL-17 in response to CpPLD. Moreover, CpPLD-specific CD4(+) T lymphocytes display helper function for monocyte MMP-9 and TF production. CpPLD promotes Th17 cell migration through the induction of chemokine secretion and adhesion molecule expression on endothelial cells. These findings indicate that CpPLD is able to drive the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 by monocytes and to elicit a Th17 immune response that plays a key role in the genesis of atherosclerosis.
Author	Della Bella, Chiara Baldari, Cosima T Mancini, Fabiola de Bernard, Marina D'Elios, Sofia Paccani, Silvia Rossi Prisco, Domenico Ciervo, Alessandra Benagiano, Marisa Munari, Fabio Ferrari, Mauro Ulivi, Camilla Amedei, Amedeo D'Elios, Mario M
Author_xml	– sequence: 1 givenname: Marisa surname: Benagiano fullname: Benagiano, Marisa organization: Patologia Medica, Azienda Ospedaliero-Universitaria Careggi Firenze, 50134 Florence, Italy – sequence: 2 givenname: Fabio surname: Munari fullname: Munari, Fabio – sequence: 3 givenname: Alessandra surname: Ciervo fullname: Ciervo, Alessandra – sequence: 4 givenname: Amedeo surname: Amedei fullname: Amedei, Amedeo – sequence: 5 givenname: Silvia Rossi surname: Paccani fullname: Paccani, Silvia Rossi – sequence: 6 givenname: Fabiola surname: Mancini fullname: Mancini, Fabiola – sequence: 7 givenname: Mauro surname: Ferrari fullname: Ferrari, Mauro – sequence: 8 givenname: Chiara surname: Della Bella fullname: Della Bella, Chiara – sequence: 9 givenname: Camilla surname: Ulivi fullname: Ulivi, Camilla – sequence: 10 givenname: Sofia surname: D'Elios fullname: D'Elios, Sofia – sequence: 11 givenname: Cosima T surname: Baldari fullname: Baldari, Cosima T – sequence: 12 givenname: Domenico surname: Prisco fullname: Prisco, Domenico – sequence: 13 givenname: Marina surname: de Bernard fullname: de Bernard, Marina – sequence: 14 givenname: Mario M surname: D'Elios fullname: D'Elios, Mario M
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/22232679$$D View this record in MEDLINE/PubMed
BookMark	eNpNUE1LxDAQDbLifujZm-SmHrrmo22ao3T9ggU9rOcy7U5ppE1i0wr77624ggPz3ht4M_BmSWbWWSTkkrM1Z0reeQthzafKpORMn5DFhDxKY81m__ScLEP4YIzpJGNnZC6EkCJVekHKvGmhO-ydb0wL1FscO2cNIPWNC1O3xkNAuqE3uX_bbm7pvjdfGOiu4YoaW0_bHQzG2WmgzdiBpTA02LtQtT9owjk5raENeHHkFXl_fNjlz9H29eklv99GVZLIISqTSkKSshJZhTyWGtKsyoCxTNeoS6kmjWlaxSrmJcIUq0aWSVQVxJCgECty_XvX9-5zxDAUnQkVti1YdGMotGBCKJXFk_Pq6BzLDveF700H_aH4e4v4BpctZ4c
CitedBy_id	crossref_primary_10_3390_toxins9040125 crossref_primary_10_4049_jimmunol_1600305 crossref_primary_10_1016_j_bpobgyn_2019_03_001 crossref_primary_10_1155_2013_142358 crossref_primary_10_1016_j_tim_2014_04_013 crossref_primary_10_1111_cmi_12947 crossref_primary_10_1002_adhm_202302054 crossref_primary_10_1007_s11906_017_0753_y crossref_primary_10_1038_srep40515 crossref_primary_10_1080_14767058_2017_1409718 crossref_primary_10_31083_j_fbl2904161 crossref_primary_10_1016_j_neubiorev_2013_01_021 crossref_primary_10_1100_2012_157534 crossref_primary_10_1093_eurheartj_ehs263 crossref_primary_10_1002_1873_3468_14156 crossref_primary_10_1007_s11481_012_9421_9 crossref_primary_10_1517_14728222_2015_1016499 crossref_primary_10_1038_jid_2012_194 crossref_primary_10_1186_1756_0500_7_230 crossref_primary_10_3390_biomedicines9101338 crossref_primary_10_1007_s11739_014_1183_3 crossref_primary_10_1016_j_cyto_2024_156795 crossref_primary_10_1007_s13317_013_0054_7 crossref_primary_10_1111_pim_12412 crossref_primary_10_1016_j_cyto_2015_03_009 crossref_primary_10_1089_jir_2019_0034 crossref_primary_10_1016_j_ijcard_2012_05_098 crossref_primary_10_1016_j_jbior_2023_101000 crossref_primary_10_1002_adhm_202304315 crossref_primary_10_1096_fj_202100927RR crossref_primary_10_1016_j_carpath_2016_09_002 crossref_primary_10_1128_MMBR_00082_15 crossref_primary_10_1111_tri_12341 crossref_primary_10_1016_j_tice_2017_04_002 crossref_primary_10_1097_MD_0000000000005516 crossref_primary_10_1111_cei_12098 crossref_primary_10_3389_fimmu_2017_01288 crossref_primary_10_1371_journal_pone_0076664
ContentType	Journal Article
DBID	CGR CUY CVF ECM EIF NPM 7X8
DOI	10.1073/pnas.1111833109
DatabaseName	Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic
DatabaseTitle	MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic
DatabaseTitleList	MEDLINE - Academic MEDLINE
Database_xml	– sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database
DeliveryMethod	no_fulltext_linktorsrc
Discipline	Sciences (General)
EISSN	1091-6490
ExternalDocumentID	22232679
Genre	Research Support, Non-U.S. Gov't Journal Article
GroupedDBID	--- -DZ -~X .55 0R~ 123 29P 2AX 2FS 2WC 4.4 53G 5RE 5VS 85S AACGO AAFWJ AANCE ABBHK ABOCM ABPLY ABPPZ ABTLG ABXSQ ABZEH ACGOD ACHIC ACIWK ACNCT ACPRK ADQXQ ADULT AENEX AEUPB AEXZC AFFNX AFOSN AFRAH ALMA_UNASSIGNED_HOLDINGS AQVQM BKOMP CGR CS3 CUY CVF D0L DCCCD DIK DU5 E3Z EBS ECM EIF EJD F5P FRP GX1 H13 HH5 HTVGU HYE IPSME JAAYA JBMMH JENOY JHFFW JKQEH JLS JLXEF JPM JSG JST KQ8 L7B LU7 MVM N9A NPM N~3 O9- OK1 P-O PNE PQQKQ R.V RHI RNA RNS RPM RXW SA0 SJN TAE TN5 UKR W8F WH7 WOQ WOW X7M XSW Y6R YBH YKV YSK ZCA ~02 ~KM 7X8 ADXHL
ID	FETCH-LOGICAL-c553t-b5c3a560be0ce1439a68c8a0089fe9b378a0e66c4741bea649fe083e7ca4a5e22
IEDL.DBID	7X8
ISICitedReferencesCount	53
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000299412600048&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	1091-6490
IngestDate	Thu Sep 04 16:39:21 EDT 2025 Thu Apr 03 07:01:51 EDT 2025
IsDoiOpenAccess	false
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	4
Language	English
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c553t-b5c3a560be0ce1439a68c8a0089fe9b378a0e66c4741bea649fe083e7ca4a5e22
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
OpenAccessLink	https://www.pnas.org/content/pnas/109/4/1222.full.pdf
PMID	22232679
PQID	920227784
PQPubID	23479
ParticipantIDs	proquest_miscellaneous_920227784 pubmed_primary_22232679
PublicationCentury	2000
PublicationDate	2012-01-24
PublicationDateYYYYMMDD	2012-01-24
PublicationDate_xml	– month: 01 year: 2012 text: 2012-01-24 day: 24
PublicationDecade	2010
PublicationPlace	United States
PublicationPlace_xml	– name: United States
PublicationTitle	Proceedings of the National Academy of Sciences - PNAS
PublicationTitleAlternate	Proc Natl Acad Sci U S A
PublicationYear	2012
References	9024145 - Circulation. 1997 Feb 4;95(3):594-9 17245604 - Naunyn Schmiedebergs Arch Pharmacol. 2007 Feb;374(5-6):399-411 15657292 - J Exp Med. 2005 Jan 17;201(2):233-40 15879154 - J Immunol. 2005 May 15;174(10):6509-17 17581588 - Nature. 2007 Jul 26;448(7152):484-7 18097011 - J Immunol. 2008 Jan 1;180(1):122-9 19302038 - Annu Rev Immunol. 2009;27:165-97 10843722 - J Immunol. 2000 Jun 15;164(12):6621-32 16008577 - Cell Microbiol. 2005 Aug;7(8):1099-108 10627494 - Clin Microbiol Rev. 2000 Jan;13(1):122-43, table of contents 9247587 - Eur J Immunol. 1997 Jul;27(7):1751-5 17433650 - Curr Opin Immunol. 2007 Jun;19(3):281-6 20226959 - Prog Cardiovasc Dis. 2010 Mar-Apr;52(5):410-28 20192806 - Annu Rev Immunol. 2010;28:445-89 10073981 - Arterioscler Thromb Vasc Biol. 1999 Mar;19(3):734-42 16648838 - Nature. 2006 May 11;441(7090):235-8 7795230 - Blood. 1995 Jul 1;86(1):250-7 16200068 - Nat Immunol. 2005 Nov;6(11):1133-41 20935201 - J Immunol. 2010 Nov 1;185(9):5619-27 7634481 - Circulation. 1995 Aug 1;92(3):657-71 9151899 - J Exp Med. 1997 May 5;185(9):1619-27 12162876 - J Interferon Cytokine Res. 2002 Jun;22(6):661-70 7690779 - J Clin Invest. 1993 Sep;92(3):1366-72 16543949 - J Clin Invest. 2006 Apr;116(4):1092-101 17486092 - Nat Immunol. 2007 Jun;8(6):639-46 19255340 - Circulation. 2009 Mar 17;119(10):1424-32 12740434 - Proc Natl Acad Sci U S A. 2003 May 27;100(11):6658-63 17375096 - Nat Immunol. 2007 Apr;8(4):345-50 10722649 - Infect Immun. 2000 Apr;68(4):2379-85 21178014 - J Immunol. 2011 Feb 1;186(3):1411-20 18975343 - Arthritis Rheum. 2008 Nov;58(11):3609-17 19397877 - Microbes Infect. 2009 Mar;11(3):367-73 17570631 - Microb Pathog. 2007 Aug-Sep;43(2-3):96-105 11114383 - Immunity. 2000 Nov;13(5):715-25 12149255 - J Biol Chem. 2002 Oct 4;277(40):37647-54 10572314 - Microbes Infect. 1999 Nov;1(13):1103-12 12829194 - Cardiovasc Res. 2003 Jul 1;59(1):234-40 15035006 - Nat Rev Microbiol. 2004 Jan;2(1):23-32
References_xml	– reference: 17570631 - Microb Pathog. 2007 Aug-Sep;43(2-3):96-105 – reference: 7795230 - Blood. 1995 Jul 1;86(1):250-7 – reference: 20192806 - Annu Rev Immunol. 2010;28:445-89 – reference: 9151899 - J Exp Med. 1997 May 5;185(9):1619-27 – reference: 17581588 - Nature. 2007 Jul 26;448(7152):484-7 – reference: 17433650 - Curr Opin Immunol. 2007 Jun;19(3):281-6 – reference: 19255340 - Circulation. 2009 Mar 17;119(10):1424-32 – reference: 20935201 - J Immunol. 2010 Nov 1;185(9):5619-27 – reference: 15035006 - Nat Rev Microbiol. 2004 Jan;2(1):23-32 – reference: 16648838 - Nature. 2006 May 11;441(7090):235-8 – reference: 9024145 - Circulation. 1997 Feb 4;95(3):594-9 – reference: 10722649 - Infect Immun. 2000 Apr;68(4):2379-85 – reference: 11114383 - Immunity. 2000 Nov;13(5):715-25 – reference: 17245604 - Naunyn Schmiedebergs Arch Pharmacol. 2007 Feb;374(5-6):399-411 – reference: 12162876 - J Interferon Cytokine Res. 2002 Jun;22(6):661-70 – reference: 10843722 - J Immunol. 2000 Jun 15;164(12):6621-32 – reference: 9247587 - Eur J Immunol. 1997 Jul;27(7):1751-5 – reference: 21178014 - J Immunol. 2011 Feb 1;186(3):1411-20 – reference: 18975343 - Arthritis Rheum. 2008 Nov;58(11):3609-17 – reference: 18097011 - J Immunol. 2008 Jan 1;180(1):122-9 – reference: 16200068 - Nat Immunol. 2005 Nov;6(11):1133-41 – reference: 7690779 - J Clin Invest. 1993 Sep;92(3):1366-72 – reference: 19302038 - Annu Rev Immunol. 2009;27:165-97 – reference: 17486092 - Nat Immunol. 2007 Jun;8(6):639-46 – reference: 16008577 - Cell Microbiol. 2005 Aug;7(8):1099-108 – reference: 7634481 - Circulation. 1995 Aug 1;92(3):657-71 – reference: 19397877 - Microbes Infect. 2009 Mar;11(3):367-73 – reference: 10572314 - Microbes Infect. 1999 Nov;1(13):1103-12 – reference: 10627494 - Clin Microbiol Rev. 2000 Jan;13(1):122-43, table of contents – reference: 12740434 - Proc Natl Acad Sci U S A. 2003 May 27;100(11):6658-63 – reference: 12149255 - J Biol Chem. 2002 Oct 4;277(40):37647-54 – reference: 20226959 - Prog Cardiovasc Dis. 2010 Mar-Apr;52(5):410-28 – reference: 12829194 - Cardiovasc Res. 2003 Jul 1;59(1):234-40 – reference: 17375096 - Nat Immunol. 2007 Apr;8(4):345-50 – reference: 15879154 - J Immunol. 2005 May 15;174(10):6509-17 – reference: 15657292 - J Exp Med. 2005 Jan 17;201(2):233-40 – reference: 16543949 - J Clin Invest. 2006 Apr;116(4):1092-101 – reference: 10073981 - Arterioscler Thromb Vasc Biol. 1999 Mar;19(3):734-42
SSID	ssj0009580
Score	2.2960036
Snippet	Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential...
SourceID	proquest pubmed
SourceType	Aggregation Database Index Database
StartPage	1222
SubjectTerms	Aged Atherosclerosis - immunology Atherosclerosis - microbiology Cell Line Chemokines - immunology Chlamydophila pneumoniae - enzymology Cytokines - immunology Enzyme-Linked Immunosorbent Assay Female Gene Expression Regulation - immunology Human Umbilical Vein Endothelial Cells Humans Male Matrix Metalloproteinase 9 - metabolism Middle Aged Monocytes - immunology Phospholipase D - immunology Phospholipase D - pharmacology Real-Time Polymerase Chain Reaction Th17 Cells - immunology Thromboplastin - metabolism Toll-Like Receptor 4 - agonists
Title	Chlamydophila pneumoniae phospholipase D (CpPLD) drives Th17 inflammation in human atherosclerosis
URI	https://www.ncbi.nlm.nih.gov/pubmed/22232679 https://www.proquest.com/docview/920227784
Volume	109
WOSCitedRecordID	wos000299412600048&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText
inHoldings	1
isFullTextHit
isPrint
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV27TsMwFLWAMrAA5Vle8sDQDlbzcGJ7QqilYoCqQ5G6RbbjKJGqJDQtEn_PdZIiFsTAECsZnETXx_ZxfHMOQvfKiamWjiQK8EBoGLtECRMQ5TKtuPXGobo2m2DTKV8sxKzNzanatMrtmFgP1HGh7TfyofCs2B3j9KF8J9Y0ym6utg4au6jjA5OxoGYL_kNzlzdiBMIlIRXOVtmH-cMyl1U9WnDfr5MRf6OX9TQzOfrnCx6jw5Zf4scGEF20Y_IT1G17cIX7rcz04BSpUQpo-IyLMs2WEpe52cA9MmlwmRYVHMushCkOj3F_VM5exgMcr6xGLZ6nLsMATKjd_PcIF7j2-sM1nSwqeDKUWXWG3iZP89EzaR0XiA4Cf01UoH0JHEgZRxtgUkKGXHMJPEEkRiifwbkJQ02BhygjIaiJAQ5nmJZUBsbzztFeXuTmEmGZCJFoof2AGSp4AMs6zbVHFWXQAGHcQ3gbxggQbbcpZG6KTRV9B7KHLpqmiMpGeSOyZMYLmbj6u_I1OgBuY9NOiEdvUCeB3mxu0b7-WGfV6q5GCpTT2esXaX_JPA
linkProvider	ProQuest
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Chlamydophila+pneumoniae+phospholipase+D+%28CpPLD%29+drives+Th17+inflammation+in+human+atherosclerosis&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+-+PNAS&rft.au=Benagiano%2C+Marisa&rft.au=Munari%2C+Fabio&rft.au=Ciervo%2C+Alessandra&rft.au=Amedei%2C+Amedeo&rft.date=2012-01-24&rft.eissn=1091-6490&rft.volume=109&rft.issue=4&rft.spage=1222&rft_id=info:doi/10.1073%2Fpnas.1111833109&rft_id=info%3Apmid%2F22232679&rft_id=info%3Apmid%2F22232679&rft.externalDocID=22232679
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1091-6490&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1091-6490&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1091-6490&client=summon