Mycobacterium tuberculosis Infection and Innate Responses in a New Model of Lung Alveolar Macrophages
Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of ( ) in humans. Nevertheless, AMs are available only in limited amounts for studies, which hamper the detailed molecular understanding of host- interactions...
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Published in | Frontiers in immunology Vol. 9; p. 438 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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12.03.2018
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Abstract | Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of
(
) in humans. Nevertheless, AMs are available only in limited amounts for
studies, which hamper the detailed molecular understanding of host-
interactions in these macrophages. The recent establishment of the self-renewing and primary Max Planck Institute (MPI) cells, functionally very close to lung AMs, opens unique opportunities for
studies of host-pathogen interactions in respiratory diseases. Here, we investigated the suitability of MPI cells as a host cell system for
infection. Bacterial, cellular, and innate immune features of MPI cells infected with
were characterized. Live bacteria were readily internalized and efficiently replicated in MPI cells, similarly to primary murine macrophages and other cell lines. MPI cells were also suitable for the determination of anti-tuberculosis (TB) drug activity. The primary innate immune response of MPI cells to live
showed significantly higher and earlier induction of the pro-inflammatory cytokines TNFα, interleukin 6 (IL-6), IL-1α, and IL-1β, as compared to stimulation with heat-killed (HK) bacteria. MPI cells previously showed a lack of induction of the anti-inflammatory cytokine IL-10 to a wide range of stimuli, including HK
. By contrast, we show here that live
is able to induce significant amounts of IL-10 in MPI cells. Autophagy experiments using light chain 3B immunostaining, as well as LysoTracker labeling of acidic vacuoles, demonstrated that MPI cells efficiently control killed
by elimination through phagolysosomes. MPI cells were also able to accumulate lipid droplets in their cytoplasm following exposure to lipoproteins. Collectively, this study establishes the MPI cells as a relevant, versatile host cell model for TB research, allowing a deeper understanding of AMs functions in this pathology. |
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AbstractList | Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of Mycobacterium tuberculosis (Mtb) in humans. Nevertheless, AMs are available only in limited amounts for in vitro studies, which hamper the detailed molecular understanding of host-Mtb interactions in these macrophages. The recent establishment of the self-renewing and primary Max Planck Institute (MPI) cells, functionally very close to lung AMs, opens unique opportunities for in vitro studies of host-pathogen interactions in respiratory diseases. Here, we investigated the suitability of MPI cells as a host cell system for Mtb infection. Bacterial, cellular, and innate immune features of MPI cells infected with Mtb were characterized. Live bacteria were readily internalized and efficiently replicated in MPI cells, similarly to primary murine macrophages and other cell lines. MPI cells were also suitable for the determination of anti-tuberculosis (TB) drug activity. The primary innate immune response of MPI cells to live Mtb showed significantly higher and earlier induction of the pro-inflammatory cytokines TNFα, interleukin 6 (IL-6), IL-1α, and IL-1β, as compared to stimulation with heat-killed (HK) bacteria. MPI cells previously showed a lack of induction of the anti-inflammatory cytokine IL-10 to a wide range of stimuli, including HK Mtb. By contrast, we show here that live Mtb is able to induce significant amounts of IL-10 in MPI cells. Autophagy experiments using light chain 3B immunostaining, as well as LysoTracker labeling of acidic vacuoles, demonstrated that MPI cells efficiently control killed Mtb by elimination through phagolysosomes. MPI cells were also able to accumulate lipid droplets in their cytoplasm following exposure to lipoproteins. Collectively, this study establishes the MPI cells as a relevant, versatile host cell model for TB research, allowing a deeper understanding of AMs functions in this pathology. Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of ( ) in humans. Nevertheless, AMs are available only in limited amounts for studies, which hamper the detailed molecular understanding of host- interactions in these macrophages. The recent establishment of the self-renewing and primary Max Planck Institute (MPI) cells, functionally very close to lung AMs, opens unique opportunities for studies of host-pathogen interactions in respiratory diseases. Here, we investigated the suitability of MPI cells as a host cell system for infection. Bacterial, cellular, and innate immune features of MPI cells infected with were characterized. Live bacteria were readily internalized and efficiently replicated in MPI cells, similarly to primary murine macrophages and other cell lines. MPI cells were also suitable for the determination of anti-tuberculosis (TB) drug activity. The primary innate immune response of MPI cells to live showed significantly higher and earlier induction of the pro-inflammatory cytokines TNFα, interleukin 6 (IL-6), IL-1α, and IL-1β, as compared to stimulation with heat-killed (HK) bacteria. MPI cells previously showed a lack of induction of the anti-inflammatory cytokine IL-10 to a wide range of stimuli, including HK . By contrast, we show here that live is able to induce significant amounts of IL-10 in MPI cells. Autophagy experiments using light chain 3B immunostaining, as well as LysoTracker labeling of acidic vacuoles, demonstrated that MPI cells efficiently control killed by elimination through phagolysosomes. MPI cells were also able to accumulate lipid droplets in their cytoplasm following exposure to lipoproteins. Collectively, this study establishes the MPI cells as a relevant, versatile host cell model for TB research, allowing a deeper understanding of AMs functions in this pathology. Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of Mycobacterium tuberculosis ( Mtb ) in humans. Nevertheless, AMs are available only in limited amounts for in vitro studies, which hamper the detailed molecular understanding of host- Mtb interactions in these macrophages. The recent establishment of the self-renewing and primary Max Planck Institute (MPI) cells, functionally very close to lung AMs, opens unique opportunities for in vitro studies of host-pathogen interactions in respiratory diseases. Here, we investigated the suitability of MPI cells as a host cell system for Mtb infection. Bacterial, cellular, and innate immune features of MPI cells infected with Mtb were characterized. Live bacteria were readily internalized and efficiently replicated in MPI cells, similarly to primary murine macrophages and other cell lines. MPI cells were also suitable for the determination of anti-tuberculosis (TB) drug activity. The primary innate immune response of MPI cells to live Mtb showed significantly higher and earlier induction of the pro-inflammatory cytokines TNFα, interleukin 6 (IL-6), IL-1α, and IL-1β, as compared to stimulation with heat-killed (HK) bacteria. MPI cells previously showed a lack of induction of the anti-inflammatory cytokine IL-10 to a wide range of stimuli, including HK Mtb . By contrast, we show here that live Mtb is able to induce significant amounts of IL-10 in MPI cells. Autophagy experiments using light chain 3B immunostaining, as well as LysoTracker labeling of acidic vacuoles, demonstrated that MPI cells efficiently control killed Mtb by elimination through phagolysosomes. MPI cells were also able to accumulate lipid droplets in their cytoplasm following exposure to lipoproteins. Collectively, this study establishes the MPI cells as a relevant, versatile host cell model for TB research, allowing a deeper understanding of AMs functions in this pathology. |
Author | Fejer, György Woo, Minjeong Delorme, Vincent Wood, Connor Kwon, Doyoon Park, Kyu-Ho Paul |
AuthorAffiliation | 1 Tuberculosis Research Laboratory, Institut Pasteur Korea , Seongnam , South Korea 3 Applied Molecular Virology, Institut Pasteur Korea , Seongnam , South Korea 2 School of Biomedical and Healthcare Sciences, Peninsula Schools of Medicine and Dentistry, Plymouth University , Plymouth , United Kingdom |
AuthorAffiliation_xml | – name: 1 Tuberculosis Research Laboratory, Institut Pasteur Korea , Seongnam , South Korea – name: 2 School of Biomedical and Healthcare Sciences, Peninsula Schools of Medicine and Dentistry, Plymouth University , Plymouth , United Kingdom – name: 3 Applied Molecular Virology, Institut Pasteur Korea , Seongnam , South Korea |
Author_xml | – sequence: 1 givenname: Minjeong surname: Woo fullname: Woo, Minjeong organization: Tuberculosis Research Laboratory, Institut Pasteur Korea, Seongnam, South Korea – sequence: 2 givenname: Connor surname: Wood fullname: Wood, Connor organization: School of Biomedical and Healthcare Sciences, Peninsula Schools of Medicine and Dentistry, Plymouth University, Plymouth, United Kingdom – sequence: 3 givenname: Doyoon surname: Kwon fullname: Kwon, Doyoon organization: Tuberculosis Research Laboratory, Institut Pasteur Korea, Seongnam, South Korea – sequence: 4 givenname: Kyu-Ho Paul surname: Park fullname: Park, Kyu-Ho Paul organization: Applied Molecular Virology, Institut Pasteur Korea, Seongnam, South Korea – sequence: 5 givenname: György surname: Fejer fullname: Fejer, György organization: School of Biomedical and Healthcare Sciences, Peninsula Schools of Medicine and Dentistry, Plymouth University, Plymouth, United Kingdom – sequence: 6 givenname: Vincent surname: Delorme fullname: Delorme, Vincent organization: Tuberculosis Research Laboratory, Institut Pasteur Korea, Seongnam, South Korea |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29593716$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1038/jcbfm.2010.96 10.1128/JVI.69.3.1473-1479.1995 10.1371/journal.ppat.1000645 10.1073/pnas.1302877110 10.1086/315771 10.1016/j.micinf.2011.05.014 10.1164/ajrccm.153.2.8564135 10.1038/srep42225 10.1128/mBio.00670-17 10.1016/j.cell.2004.11.038 10.1093/femspd/ftw052 10.1038/mi.2011.13 10.1016/j.tube.2013.07.004 10.1128/IAI.01196-13 10.1038/nri3600 10.1165/rcmb.2010-0319OC 10.1016/j.imbio.2014.11.005 10.1073/pnas.1210500109 10.1002/eji.201040433 10.3389/fcimb.2016.00122 10.1186/1478-811X-11-60 10.1007/s00204-014-1265-z 10.1371/journal.ppat.1001100 10.1038/nature13489 10.3389/fcimb.2013.00062 10.1038/s41598-017-12623-w 10.1083/jcb.38.2.377 10.1038/ni.1781 10.21775/cimb.021.063 10.4049/jimmunol.148.6.1792 10.1007/978-1-59745-157-4_4 10.1371/journal.ppat.1000474 10.1146/annurev.immunol.021908.132612 10.1016/j.cell.2011.02.022 10.1126/science.1242974 |
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Keywords | foamy macrophage autophagy Mycobacterium tuberculosis cytokine secretion alveolar macrophages Max Planck Institute cells innate response |
Language | English |
License | This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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References | Gazzinelli (B30) 1992; 148 Hussell (B5) 2014; 14 Halbert (B15) 1995; 69 Law (B29) 1996; 153 Tanida (B22) 2008 Dinarello (B36) 2009; 27 Redford (B32) 2010; 40 Fejer (B9) 2013; 110 Boorsma (B11) 2017; 7 Mendoza-Coronel (B16) 2016; 74 Russell (B2) 2009; 10 Fejer (B8) 2015; 220 Castillo (B20) 2012; 109 Liang (B21) 2017; 21 Caire-Brändli (B26) 2014; 82 Bowdish (B33) 2009; 5 Cooper (B34) 2011; 4 Christophe (B18) 2009; 5 Santucci (B25) 2016; 6 Orme (B3) 2014; 94 Briken (B35) 2013; 3 Hsiao (B14) 2011; 13 Subbian (B4) 2013; 11 Sjogren (B13) 2014; 88 Brodin (B24) 2010; 6 Fedorko (B23) 1968; 38 Steiner (B12) 2011; 31 Adams (B6) 2011; 145 Maler (B10) 2017; 8 O’leary (B31) 2011; 45 (B1) 2016 Sieweke (B7) 2013; 342 Juffermans (B27) 2000; 182 Andreu (B17) 2017; 7 Mayer-Barber (B28) 2014; 511 Gutierrez (B19) 2004; 119 |
References_xml | – volume: 31 start-page: 315 year: 2011 ident: B12 article-title: Comparison of immortalized bEnd5 and primary mouse brain microvascular endothelial cells as in vitro blood–brain barrier models for the study of T cell extravasation publication-title: J Cereb Blood Flow Metab doi: 10.1038/jcbfm.2010.96 contributor: fullname: Steiner – volume-title: Global Tuberculosis Report 2016 year: 2016 ident: B1 – volume: 69 start-page: 1473 year: 1995 ident: B15 article-title: Adeno-associated virus vectors transduce primary cells much less efficiently than immortalized cells publication-title: J Virol doi: 10.1128/JVI.69.3.1473-1479.1995 contributor: fullname: Halbert – volume: 5 start-page: e1000645 year: 2009 ident: B18 article-title: High content screening identifies decaprenyl-phosphoribose 2′ epimerase as a target for intracellular antimycobacterial inhibitors publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1000645 contributor: fullname: Christophe – volume: 110 start-page: E2191 year: 2013 ident: B9 article-title: Nontransformed, GM-CSF-dependent macrophage lines are a unique model to study tissue macrophage functions publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1302877110 contributor: fullname: Fejer – volume: 182 start-page: 902 year: 2000 ident: B27 article-title: Interleukin-1 signaling is essential for host defense during murine pulmonary tuberculosis publication-title: J Infect Dis doi: 10.1086/315771 contributor: fullname: Juffermans – volume: 13 start-page: 1033 year: 2011 ident: B14 article-title: The effects of macrophage source on the mechanism of phagocytosis and intracellular survival of Leishmania publication-title: Microbes Infect doi: 10.1016/j.micinf.2011.05.014 contributor: fullname: Hsiao – volume: 153 start-page: 799 year: 1996 ident: B29 article-title: Increased release of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha by bronchoalveolar cells lavaged from involved sites in pulmonary tuberculosis publication-title: Am J Respir Crit Care Med doi: 10.1164/ajrccm.153.2.8564135 contributor: fullname: Law – volume: 7 start-page: 42225 year: 2017 ident: B17 article-title: Primary macrophages and J774 cells respond differently to infection with Mycobacterium tuberculosis publication-title: Sci Rep doi: 10.1038/srep42225 contributor: fullname: Andreu – volume: 8 start-page: e00670 year: 2017 ident: B10 article-title: Key role of the scavenger receptor MARCO in mediating adenovirus infection and subsequent innate responses of macrophages publication-title: mBio doi: 10.1128/mBio.00670-17 contributor: fullname: Maler – volume: 119 start-page: 753 year: 2004 ident: B19 article-title: Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages publication-title: Cell doi: 10.1016/j.cell.2004.11.038 contributor: fullname: Gutierrez – volume: 74 year: 2016 ident: B16 article-title: Comparative evaluation of in vitro human macrophage models for mycobacterial infection study publication-title: Pathog Dis doi: 10.1093/femspd/ftw052 contributor: fullname: Mendoza-Coronel – volume: 4 start-page: 252 year: 2011 ident: B34 article-title: Role of innate cytokines in mycobacterial infection publication-title: Mucosal Immunol doi: 10.1038/mi.2011.13 contributor: fullname: Cooper – volume: 94 start-page: 8 year: 2014 ident: B3 article-title: A new unifying theory of the pathogenesis of tuberculosis publication-title: Tuberculosis doi: 10.1016/j.tube.2013.07.004 contributor: fullname: Orme – volume: 82 start-page: 476 year: 2014 ident: B26 article-title: Reversible lipid accumulation and associated division arrest of Mycobacterium avium in lipoprotein-induced foamy macrophages may resemble key events during latency and reactivation of tuberculosis publication-title: Infect Immun doi: 10.1128/IAI.01196-13 contributor: fullname: Caire-Brändli – volume: 14 start-page: 81 year: 2014 ident: B5 article-title: Alveolar macrophages: plasticity in a tissue-specific context publication-title: Nat Rev Immunol doi: 10.1038/nri3600 contributor: fullname: Hussell – volume: 45 start-page: 172 year: 2011 ident: B31 article-title: IL-10 blocks phagosome maturation in Mycobacterium tuberculosis-infected human macrophages publication-title: Am J Respir Cell Mol Biol doi: 10.1165/rcmb.2010-0319OC contributor: fullname: O’leary – volume: 220 start-page: 169 year: 2015 ident: B8 article-title: Self-renewing macrophages – a new line of enquiries in mononuclear phagocytes publication-title: Immunobiology doi: 10.1016/j.imbio.2014.11.005 contributor: fullname: Fejer – volume: 109 start-page: E3168 year: 2012 ident: B20 article-title: Autophagy protects against active tuberculosis by suppressing bacterial burden and inflammation publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1210500109 contributor: fullname: Castillo – volume: 40 start-page: 2200 year: 2010 ident: B32 article-title: Enhanced protection to Mycobacterium tuberculosis infection in IL-10-deficient mice is accompanied by early and enhanced Th1 responses in the lung publication-title: Eur J Immunol doi: 10.1002/eji.201040433 contributor: fullname: Redford – volume: 6 start-page: 122 year: 2016 ident: B25 article-title: Experimental models of foamy macrophages and approaches for dissecting the mechanisms of lipid accumulation and consumption during dormancy and reactivation of tuberculosis publication-title: Front Cell Infect Microbiol doi: 10.3389/fcimb.2016.00122 contributor: fullname: Santucci – volume: 11 start-page: 60 year: 2013 ident: B4 article-title: Early innate immunity determines outcome of Mycobacterium tuberculosis pulmonary infection in rabbits publication-title: Cell Commun Signal doi: 10.1186/1478-811X-11-60 contributor: fullname: Subbian – volume: 88 start-page: 1427 year: 2014 ident: B13 article-title: Critical differences in toxicity mechanisms in induced pluripotent stem cell-derived hepatocytes, hepatic cell lines and primary hepatocytes publication-title: Arch Toxicol doi: 10.1007/s00204-014-1265-z contributor: fullname: Sjogren – volume: 6 start-page: e1001100 year: 2010 ident: B24 article-title: High content phenotypic cell-based visual screen identifies Mycobacterium tuberculosis acyltrehalose-containing glycolipids involved in phagosome remodeling publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1001100 contributor: fullname: Brodin – volume: 511 start-page: 99 year: 2014 ident: B28 article-title: Host-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalk publication-title: Nature doi: 10.1038/nature13489 contributor: fullname: Mayer-Barber – volume: 3 start-page: 62 year: 2013 ident: B35 article-title: Mycobacterium tuberculosis and the host cell inflammasome: a complex relationship publication-title: Front Cell Infect Microbiol doi: 10.3389/fcimb.2013.00062 contributor: fullname: Briken – volume: 7 start-page: 12570 year: 2017 ident: B11 article-title: A potent tartrate resistant acid phosphatase inhibitor to study the function of TRAP in alveolar macrophages publication-title: Sci Rep doi: 10.1038/s41598-017-12623-w contributor: fullname: Boorsma – volume: 38 start-page: 377 year: 1968 ident: B23 article-title: Autophagic vacuoles produced in vitro: I. Studies on cultured macrophages exposed to chloroquine publication-title: J Cell Biol doi: 10.1083/jcb.38.2.377 contributor: fullname: Fedorko – volume: 10 start-page: 943 year: 2009 ident: B2 article-title: Foamy macrophages and the progression of the human tuberculosis granuloma publication-title: Nat Immunol doi: 10.1038/ni.1781 contributor: fullname: Russell – volume: 21 start-page: 63 year: 2017 ident: B21 article-title: Mycobacteria and autophagy: many questions and few answers publication-title: Curr Issues Mol Biol doi: 10.21775/cimb.021.063 contributor: fullname: Liang – volume: 148 start-page: 1792 year: 1992 ident: B30 article-title: IL-10 inhibits parasite killing and nitrogen oxide production by IFN-gamma-activated macrophages publication-title: J Immunol doi: 10.4049/jimmunol.148.6.1792 contributor: fullname: Gazzinelli – start-page: 77 volume-title: Autophagosome and Phagosome year: 2008 ident: B22 article-title: LC3 and autophagy doi: 10.1007/978-1-59745-157-4_4 contributor: fullname: Tanida – volume: 5 start-page: e1000474 year: 2009 ident: B33 article-title: MARCO, TLR2, and CD14 are required for macrophage cytokine responses to mycobacterial trehalose dimycolate and Mycobacterium tuberculosis publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1000474 contributor: fullname: Bowdish – volume: 27 start-page: 519 year: 2009 ident: B36 article-title: Immunological and inflammatory functions of the interleukin-1 family publication-title: Annu Rev Immunol doi: 10.1146/annurev.immunol.021908.132612 contributor: fullname: Dinarello – volume: 145 start-page: 39 year: 2011 ident: B6 article-title: Drug tolerance in replicating mycobacteria mediated by a macrophage-induced efflux mechanism publication-title: Cell doi: 10.1016/j.cell.2011.02.022 contributor: fullname: Adams – volume: 342 start-page: 1242974 year: 2013 ident: B7 article-title: Beyond stem cells: self-renewal of differentiated macrophages publication-title: Science doi: 10.1126/science.1242974 contributor: fullname: Sieweke |
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Snippet | Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of
(
) in humans.... Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of Mycobacterium... Lung alveolar macrophages (AMs) are in the first line of immune defense against respiratory pathogens and play key roles in the pathogenesis of Mycobacterium... |
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StartPage | 438 |
SubjectTerms | alveolar macrophages autophagy cytokine secretion Immunology innate response Max Planck Institute cells Mycobacterium tuberculosis |
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Title | Mycobacterium tuberculosis Infection and Innate Responses in a New Model of Lung Alveolar Macrophages |
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