Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular Traps
Tuberculosis is one of the leading causes of human morbidity and mortality. Mycobacterium tuberculosis (Mtb) employs different strategies to evade and counterattack immune responses persisting for years. Mast cells are crucial during innate immune responses and help clear infections via inflammation...
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Frontiers Media S.A.
2018-05-01
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Online Access: | https://www.frontiersin.org/article/10.3389/fimmu.2018.01161/full |
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author | Marcia Campillo-Navarro Marcia Campillo-Navarro Kahiry Leyva-Paredes Luis Donis-Maturano Gloria M. Rodríguez-López Rodolfo Soria-Castro Blanca Estela García-Pérez Nahum Puebla-Osorio Stephen E. Ullrich Stephen E. Ullrich Julieta Luna-Herrera Leopoldo Flores-Romo Héctor Sumano-López Sonia M. Pérez-Tapia Sonia M. Pérez-Tapia Sergio Estrada-Parra Iris Estrada-García Rommel Chacón-Salinas Rommel Chacón-Salinas |
author_facet | Marcia Campillo-Navarro Marcia Campillo-Navarro Kahiry Leyva-Paredes Luis Donis-Maturano Gloria M. Rodríguez-López Rodolfo Soria-Castro Blanca Estela García-Pérez Nahum Puebla-Osorio Stephen E. Ullrich Stephen E. Ullrich Julieta Luna-Herrera Leopoldo Flores-Romo Héctor Sumano-López Sonia M. Pérez-Tapia Sonia M. Pérez-Tapia Sergio Estrada-Parra Iris Estrada-García Rommel Chacón-Salinas Rommel Chacón-Salinas |
author_sort | Marcia Campillo-Navarro |
collection | DOAJ |
description | Tuberculosis is one of the leading causes of human morbidity and mortality. Mycobacterium tuberculosis (Mtb) employs different strategies to evade and counterattack immune responses persisting for years. Mast cells are crucial during innate immune responses and help clear infections via inflammation or by direct antibacterial activity through extracellular traps (MCETs). Whether Mtb induce MCETs production is unknown. In this study, we report that viable Mtb did not induce DNA release by mast cells, but heat-killed Mtb (HK-Mtb) did. DNA released by mast cells after stimulation with HK-Mtb was complexed with histone and tryptase. MCETs induced with PMA and HK-Mtb were unable to kill live Mtb bacilli. Mast cells stimulated with HK-Mtb induced hydrogen peroxide production, whereas cells stimulated with viable Mtb did not. Moreover, MCETs induction by HK-Mtb was dependent of NADPH oxidase activity, because its blockade resulted in a diminished DNA release by mast cells. Interestingly, catalase-deficient Mtb induced a significant production of hydrogen peroxide and DNA release by mast cells, indicating that catalase produced by Mtb prevents MCETs release by degrading hydrogen peroxide. Our findings show a new strategy employed by Mtb to overcome the immune response through inhibiting MCETs formation, which could be relevant during early stages of infection. |
first_indexed | 2024-12-23T06:04:03Z |
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issn | 1664-3224 |
language | English |
last_indexed | 2024-12-23T06:04:03Z |
publishDate | 2018-05-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Immunology |
spelling | doaj.art-4c42bfee889143aba5af4894b04fae6a2022-12-21T17:57:37ZengFrontiers Media S.A.Frontiers in Immunology1664-32242018-05-01910.3389/fimmu.2018.01161362701Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular TrapsMarcia Campillo-Navarro0Marcia Campillo-Navarro1Kahiry Leyva-Paredes2Luis Donis-Maturano3Gloria M. Rodríguez-López4Rodolfo Soria-Castro5Blanca Estela García-Pérez6Nahum Puebla-Osorio7Stephen E. Ullrich8Stephen E. Ullrich9Julieta Luna-Herrera10Leopoldo Flores-Romo11Héctor Sumano-López12Sonia M. Pérez-Tapia13Sonia M. Pérez-Tapia14Sergio Estrada-Parra15Iris Estrada-García16Rommel Chacón-Salinas17Rommel Chacón-Salinas18Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartamento de Fisiología y Farmacología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, UNAM, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartment of Cell Biology, Cinvestav, Instituto Politécnico Nacional, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, United StatesDepartment of Immunology, The Center for Cancer Immunology Research, The University of Texas MD Anderson Cancer Center, Houston, TX, United StatesThe University of Texas Graduate School of Biological Sciences at Houston, Houston, TX, United StatesDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartment of Cell Biology, Cinvestav, Instituto Politécnico Nacional, México City, MexicoDepartamento de Fisiología y Farmacología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, UNAM, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoUnidad de Desarrollo e Investigación en Bioprocesos (UDIBI), Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoUnidad de Desarrollo e Investigación en Bioprocesos (UDIBI), Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, México City, MexicoTuberculosis is one of the leading causes of human morbidity and mortality. Mycobacterium tuberculosis (Mtb) employs different strategies to evade and counterattack immune responses persisting for years. Mast cells are crucial during innate immune responses and help clear infections via inflammation or by direct antibacterial activity through extracellular traps (MCETs). Whether Mtb induce MCETs production is unknown. In this study, we report that viable Mtb did not induce DNA release by mast cells, but heat-killed Mtb (HK-Mtb) did. DNA released by mast cells after stimulation with HK-Mtb was complexed with histone and tryptase. MCETs induced with PMA and HK-Mtb were unable to kill live Mtb bacilli. Mast cells stimulated with HK-Mtb induced hydrogen peroxide production, whereas cells stimulated with viable Mtb did not. Moreover, MCETs induction by HK-Mtb was dependent of NADPH oxidase activity, because its blockade resulted in a diminished DNA release by mast cells. Interestingly, catalase-deficient Mtb induced a significant production of hydrogen peroxide and DNA release by mast cells, indicating that catalase produced by Mtb prevents MCETs release by degrading hydrogen peroxide. Our findings show a new strategy employed by Mtb to overcome the immune response through inhibiting MCETs formation, which could be relevant during early stages of infection.https://www.frontiersin.org/article/10.3389/fimmu.2018.01161/fulltuberculosisMycobacterium tuberculosismast cellmast cell extracellular trapcatalase |
spellingShingle | Marcia Campillo-Navarro Marcia Campillo-Navarro Kahiry Leyva-Paredes Luis Donis-Maturano Gloria M. Rodríguez-López Rodolfo Soria-Castro Blanca Estela García-Pérez Nahum Puebla-Osorio Stephen E. Ullrich Stephen E. Ullrich Julieta Luna-Herrera Leopoldo Flores-Romo Héctor Sumano-López Sonia M. Pérez-Tapia Sonia M. Pérez-Tapia Sergio Estrada-Parra Iris Estrada-García Rommel Chacón-Salinas Rommel Chacón-Salinas Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular Traps Frontiers in Immunology tuberculosis Mycobacterium tuberculosis mast cell mast cell extracellular trap catalase |
title | Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular Traps |
title_full | Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular Traps |
title_fullStr | Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular Traps |
title_full_unstemmed | Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular Traps |
title_short | Mycobacterium tuberculosis Catalase Inhibits the Formation of Mast Cell Extracellular Traps |
title_sort | mycobacterium tuberculosis catalase inhibits the formation of mast cell extracellular traps |
topic | tuberculosis Mycobacterium tuberculosis mast cell mast cell extracellular trap catalase |
url | https://www.frontiersin.org/article/10.3389/fimmu.2018.01161/full |
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