In vivo protective role of human group IIa phospholipase A2 against experimental anthrax
Anthrax is an acute disease caused by Bacillus anthracis. Some animal species are relatively resistant to anthrax infection. This trait has been correlated to the extent of the local inflammatory reaction, suggesting innate immunity to be the first line of defense against B. anthracis infection in n...
Saved in:
| Published in: | The Journal of immunology (1950) Vol. 175; no. 10; p. 6786 |
|---|---|
| Main Authors: | , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
United States
15.11.2005
|
| Subjects: | |
| ISSN: | 0022-1767 |
| Online Access: | Get more information |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Abstract | Anthrax is an acute disease caused by Bacillus anthracis. Some animal species are relatively resistant to anthrax infection. This trait has been correlated to the extent of the local inflammatory reaction, suggesting innate immunity to be the first line of defense against B. anthracis infection in nonimmunized hosts. Group IIA secreted phospholipase A2 (sPLA2-IIA) is produced in particular by macrophages and possesses potent antibacterial activity especially against Gram-positive bacteria. We have previously shown in vitro that sPLA2-IIA kills both germinated B. anthracis spores and encapsulated bacilli. Here we show that sPLA2-IIA plays in vivo a protective role against experimental anthrax. Transgenic mice expressing human sPLA2-IIA are resistant to B. anthracis infection. In addition, in vivo administration of recombinant human sPLA2-IIA protects mice against B. anthracis infection. The protective effect was observed both with a highly virulent encapsulated nontoxinogenic strain and a wild-type encapsulated toxinogenic strain, showing that toxemia did not hinder the sPLA2-IIA-afforded protection. sPLA2-IIA, a natural component of the immune system, may thus be considered a novel therapeutic agent to be used in adjunct with current therapy for treating anthrax. Its anthracidal activity would be effective even against strains resistant to multiple antibiotics. |
|---|---|
| AbstractList | Anthrax is an acute disease caused by Bacillus anthracis. Some animal species are relatively resistant to anthrax infection. This trait has been correlated to the extent of the local inflammatory reaction, suggesting innate immunity to be the first line of defense against B. anthracis infection in nonimmunized hosts. Group IIA secreted phospholipase A2 (sPLA2-IIA) is produced in particular by macrophages and possesses potent antibacterial activity especially against Gram-positive bacteria. We have previously shown in vitro that sPLA2-IIA kills both germinated B. anthracis spores and encapsulated bacilli. Here we show that sPLA2-IIA plays in vivo a protective role against experimental anthrax. Transgenic mice expressing human sPLA2-IIA are resistant to B. anthracis infection. In addition, in vivo administration of recombinant human sPLA2-IIA protects mice against B. anthracis infection. The protective effect was observed both with a highly virulent encapsulated nontoxinogenic strain and a wild-type encapsulated toxinogenic strain, showing that toxemia did not hinder the sPLA2-IIA-afforded protection. sPLA2-IIA, a natural component of the immune system, may thus be considered a novel therapeutic agent to be used in adjunct with current therapy for treating anthrax. Its anthracidal activity would be effective even against strains resistant to multiple antibiotics. Anthrax is an acute disease caused by Bacillus anthracis. Some animal species are relatively resistant to anthrax infection. This trait has been correlated to the extent of the local inflammatory reaction, suggesting innate immunity to be the first line of defense against B. anthracis infection in nonimmunized hosts. Group IIA secreted phospholipase A2 (sPLA2-IIA) is produced in particular by macrophages and possesses potent antibacterial activity especially against Gram-positive bacteria. We have previously shown in vitro that sPLA2-IIA kills both germinated B. anthracis spores and encapsulated bacilli. Here we show that sPLA2-IIA plays in vivo a protective role against experimental anthrax. Transgenic mice expressing human sPLA2-IIA are resistant to B. anthracis infection. In addition, in vivo administration of recombinant human sPLA2-IIA protects mice against B. anthracis infection. The protective effect was observed both with a highly virulent encapsulated nontoxinogenic strain and a wild-type encapsulated toxinogenic strain, showing that toxemia did not hinder the sPLA2-IIA-afforded protection. sPLA2-IIA, a natural component of the immune system, may thus be considered a novel therapeutic agent to be used in adjunct with current therapy for treating anthrax. Its anthracidal activity would be effective even against strains resistant to multiple antibiotics.Anthrax is an acute disease caused by Bacillus anthracis. Some animal species are relatively resistant to anthrax infection. This trait has been correlated to the extent of the local inflammatory reaction, suggesting innate immunity to be the first line of defense against B. anthracis infection in nonimmunized hosts. Group IIA secreted phospholipase A2 (sPLA2-IIA) is produced in particular by macrophages and possesses potent antibacterial activity especially against Gram-positive bacteria. We have previously shown in vitro that sPLA2-IIA kills both germinated B. anthracis spores and encapsulated bacilli. Here we show that sPLA2-IIA plays in vivo a protective role against experimental anthrax. Transgenic mice expressing human sPLA2-IIA are resistant to B. anthracis infection. In addition, in vivo administration of recombinant human sPLA2-IIA protects mice against B. anthracis infection. The protective effect was observed both with a highly virulent encapsulated nontoxinogenic strain and a wild-type encapsulated toxinogenic strain, showing that toxemia did not hinder the sPLA2-IIA-afforded protection. sPLA2-IIA, a natural component of the immune system, may thus be considered a novel therapeutic agent to be used in adjunct with current therapy for treating anthrax. Its anthracidal activity would be effective even against strains resistant to multiple antibiotics. |
| Author | Piris-Gimenez, Alejandro Paya, Miguel Chignard, Michel Touqui, Lhousseine Mock, Michèle Goossens, Pierre L Lambeau, Gérard |
| Author_xml | – sequence: 1 givenname: Alejandro surname: Piris-Gimenez fullname: Piris-Gimenez, Alejandro organization: Unité Toxines et Pathogénie Bactérienne/Centre National de la Recherche Scientifique Unité de Recherche Associée 2172, Paris, France – sequence: 2 givenname: Miguel surname: Paya fullname: Paya, Miguel – sequence: 3 givenname: Gérard surname: Lambeau fullname: Lambeau, Gérard – sequence: 4 givenname: Michel surname: Chignard fullname: Chignard, Michel – sequence: 5 givenname: Michèle surname: Mock fullname: Mock, Michèle – sequence: 6 givenname: Lhousseine surname: Touqui fullname: Touqui, Lhousseine – sequence: 7 givenname: Pierre L surname: Goossens fullname: Goossens, Pierre L |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16272335$$D View this record in MEDLINE/PubMed |
| BookMark | eNo1UE1Lw0AU3EPFfug_ENmTt9TNbvI2OZaiNVDwouAtvGxe2pRkN2aTUv-9AethGBiGYWaWbGadJcYeQrGORJQ-n-q2Ha1r1qGO15MIOoEZWwghZRBq0HO29P4khAAho1s2D0FqqVS8YF-Z5ef67HjXu4HMUJ-J964h7ip-HFu0_NC7seNZhrw7Oj-hqTv0xDeS4wFr6wdOl476uiU7YMPRDsceL3fspsLG0_2VV-zz9eVj-xbs33fZdrMPjEpTCLQQKYGOQFFlZKkKgyoW2gCJBFNtNGqtwiICCgsI46IkwAplFFUiVQZKuWJPf7nTgO-R_JC3tTfUNGjJjT6HRAMkMUzGx6txLFoq825qjP1P_v-F_AV-w2OK |
| CitedBy_id | crossref_primary_10_1128_IAI_00059_08 crossref_primary_10_1128_microbiolspec_TBS_0001_2012 crossref_primary_10_1002_emmm_201000072 crossref_primary_10_1155_2014_689815 crossref_primary_10_1021_bi061376d crossref_primary_10_1371_journal_ppat_0030187 crossref_primary_10_1155_2011_925012 crossref_primary_10_1093_infdis_jis686 crossref_primary_10_4049_jimmunol_1100499 crossref_primary_10_1111_j_1462_5822_2006_00806_x crossref_primary_10_1146_annurev_biochem_76_062405_154007 crossref_primary_10_1586_14787210_5_4_665 crossref_primary_10_1016_j_bbalip_2006_05_011 crossref_primary_10_1016_j_biochi_2010_03_015 crossref_primary_10_1128_IAI_00556_19 crossref_primary_10_4049_jimmunol_1402665 crossref_primary_10_2217_17460913_1_4_397 crossref_primary_10_1074_jbc_M611883200 crossref_primary_10_1128_AAC_00741_07 crossref_primary_10_1161_CIRCULATIONAHA_110_936393 crossref_primary_10_1182_blood_2006_10_052258 crossref_primary_10_1002_mbo3_109 crossref_primary_10_1016_j_biochi_2010_01_024 crossref_primary_10_1128_IAI_00180_18 crossref_primary_10_1021_jm901024b crossref_primary_10_3389_fphar_2020_01096 crossref_primary_10_1128_JB_01221_06 crossref_primary_10_3389_fimmu_2020_01198 crossref_primary_10_1128_JB_188_10_3433_3441_2006 crossref_primary_10_1016_j_biochi_2021_06_009 crossref_primary_10_4049_jimmunol_176_8_4987 crossref_primary_10_1016_j_bcp_2009_11_023 crossref_primary_10_2492_inflammregen_28_454 crossref_primary_10_1016_j_bbalip_2018_08_017 crossref_primary_10_3109_14767058_2013_847918 crossref_primary_10_1111_j_1365_3083_2009_02284_x crossref_primary_10_1194_jlr_R058123 crossref_primary_10_1111_j_1365_2249_2009_03893_x crossref_primary_10_1016_j_jaci_2009_04_035 crossref_primary_10_4049_jimmunol_181_7_4989 crossref_primary_10_1371_journal_ppat_1007348 crossref_primary_10_1038_ncomms6105 crossref_primary_10_1007_s10557_008_6134_7 crossref_primary_10_1016_j_ijmm_2007_09_007 crossref_primary_10_1111_imr_13205 crossref_primary_10_1093_jb_mvr088 crossref_primary_10_1016_j_tibs_2009_08_003 crossref_primary_10_1074_jbc_M109_070797 crossref_primary_10_1016_j_micres_2013_02_005 crossref_primary_10_1186_s41936_020_00167_x crossref_primary_10_1016_j_biochi_2012_09_007 crossref_primary_10_1016_j_it_2020_02_003 crossref_primary_10_4049_jimmunol_0803406 crossref_primary_10_1016_j_plipres_2010_12_001 crossref_primary_10_3390_toxins16020066 |
| ContentType | Journal Article |
| DBID | CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.4049/jimmunol.175.10.6786 |
| 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 MEDLINE - Academic |
| 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 | Medicine Biology |
| ExternalDocumentID | 16272335 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GroupedDBID | --- -~X .55 .GJ 18M 2WC 34G 39C 3O- 53G 5GY 5RE 5VS 5WD 79B 85S AARDX ABCQX ABDFA ABDPE ABEFU ABGNP ABJNI ABOCM ABPPZ ACGFO ACGFS ACIWK ACNCT ACPRK ADBBV ADIPN ADNWM AENEX AFFNX AFHIN AFOSN AFRAH AHMMS AHWXS AI. AIZAD ALMA_UNASSIGNED_HOLDINGS BAWUL BTFSW CGR CUY CVF D0L DIK DU5 E3Z EBS ECM EIF EJD F5P FRP GX1 H13 IH2 J5H K-O KQ8 L7B MVM NEJ NPM OCZFY OK1 OWPYF P0W P2P PQQKQ R.V RHF RHI ROX RZQ SJN TR2 TWZ VH1 VXZ W8F WH7 WOQ X7M XJT XSW XTH YHG YIN ZE2 ZGI 0R~ 7X8 ABEJV ABXVV ADXHL AETEA ARBBW BCRHZ KOP |
| ID | FETCH-LOGICAL-c3996-7009e67463efc2d3bca3507c6e08a97c7a7731b46e1b615bde6afa244f093c6d2 |
| IEDL.DBID | 7X8 |
| ISSN | 0022-1767 |
| IngestDate | Wed Oct 01 14:35:22 EDT 2025 Wed Feb 19 02:35:26 EST 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 10 |
| Language | English |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c3996-7009e67463efc2d3bca3507c6e08a97c7a7731b46e1b615bde6afa244f093c6d2 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://www.jimmunol.org/content/jimmunol/175/10/6786.full.pdf |
| PMID | 16272335 |
| PQID | 68766856 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_68766856 pubmed_primary_16272335 |
| PublicationCentury | 2000 |
| PublicationDate | 2005-11-15 |
| PublicationDateYYYYMMDD | 2005-11-15 |
| PublicationDate_xml | – month: 11 year: 2005 text: 2005-11-15 day: 15 |
| PublicationDecade | 2000 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | The Journal of immunology (1950) |
| PublicationTitleAlternate | J Immunol |
| PublicationYear | 2005 |
| SSID | ssj0006024 |
| Score | 2.0932608 |
| Snippet | Anthrax is an acute disease caused by Bacillus anthracis. Some animal species are relatively resistant to anthrax infection. This trait has been correlated to... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | 6786 |
| SubjectTerms | Animals Anthrax - immunology Anthrax - prevention & control Anthrax - therapy Bacillus anthracis - immunology Bacillus anthracis - pathogenicity Female Group II Phospholipases A2 Humans Immunity, Innate Mice Mice, Inbred C57BL Mice, Transgenic Phospholipases A - genetics Phospholipases A - immunology Phospholipases A - pharmacology Phospholipases A2 Recombinant Proteins - genetics Recombinant Proteins - immunology Recombinant Proteins - pharmacology |
| Title | In vivo protective role of human group IIa phospholipase A2 against experimental anthrax |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/16272335 https://www.proquest.com/docview/68766856 |
| Volume | 175 |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1NT9wwEB3xrV4ohUKhLfWBa2ATOzOJhIRQVdQ9sOLQSntb2Y4NQatky8IK_j3jfAguqAcOyc1SNBnPPHtm3gM4QkNOKZNFKXkfqYIGkUnQR4X1mPEvp7QwjdgEjUbZeJxfLcFpPwsT2ir7mNgE6qK24Y78BHnbYpbi2exfFDSjQm21E9BYhlXJQCY0dNH4hSscB4nqucJjQmoH5xRD4pPbMgxf1NNjTp58fj3miI1vQ8wm1Vx8fN9HbsFmBzHFeesTn2DJVduw3opOPm3DxmVXTt-B8bASi3JRi46tgSOfCO2GovaiEe8TzdCHGA61mN3Uc36m5YzznjhPhL7WJWNL8VojQOigu6AfP8Pfi19_fv6OOqmFyMrQhkwMtRySQum8TQpprJaMFC26QaZzsqSJZGwUutgwBjKFQ-01QwM_yKXFItmFlaqu3BcQXuUktSnQU6Z8zKuVl4aoQSOYu3340dtuwq4c6hO6cvXDfNJbbx_2WvNPZi3jxiTGhBIp04P_rv0KH1py1TiK02-w6nkTu--wZhf35fzusPEQfo-uLp8BkAzGZw |
| 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=In+vivo+protective+role+of+human+group+IIa+phospholipase+A2+against+experimental+anthrax&rft.jtitle=The+Journal+of+immunology+%281950%29&rft.au=Piris-Gimenez%2C+Alejandro&rft.au=Paya%2C+Miguel&rft.au=Lambeau%2C+G%C3%A9rard&rft.au=Chignard%2C+Michel&rft.date=2005-11-15&rft.issn=0022-1767&rft.volume=175&rft.issue=10&rft.spage=6786&rft_id=info:doi/10.4049%2Fjimmunol.175.10.6786&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-1767&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-1767&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-1767&client=summon |