---
_id: '3161'
abstract:
- lang: eng
  text: 'Some inflammatory stimuli trigger activation of the NLRP3 inflammasome by
    inducing efflux of cellular potassium. Loss of cellular potassium is known to
    potently suppress protein synthesis, leading us to test whether the inhibition
    of protein synthesis itself serves as an activating signal for the NLRP3 inflammasome.
    Murine bone marrow-derived macrophages, either primed by LPS or unprimed, were
    exposed to a panel of inhibitors of ribosomal function: ricin, cycloheximide,
    puromycin, pactamycin, and anisomycin. Macrophages were also exposed to nigericin,
    ATP, monosodium urate (MSU), and poly I:C. Synthesis of pro-IL-ß and release of
    IL-1ß from cells in response to these agents was detected by immunoblotting and
    ELISA. Release of intracellular potassium was measured by mass spectrometry. Inhibition
    of translation by each of the tested translation inhibitors led to processing
    of IL-1ß, which was released from cells. Processing and release of IL-1ß was reduced
    or absent from cells deficient in NLRP3, ASC, or caspase-1, demonstrating the
    role of the NLRP3 inflammasome. Despite the inability of these inhibitors to trigger
    efflux of intracellular potassium, the addition of high extracellular potassium
    suppressed activation of the NLRP3 inflammasome. MSU and double-stranded RNA,
    which are known to activate the NLRP3 inflammasome, also substantially inhibited
    protein translation, supporting a close association between inhibition of translation
    and inflammasome activation. These data demonstrate that translational inhibition
    itself constitutes a heretofore-unrecognized mechanism underlying IL-1ß dependent
    inflammatory signaling and that other physical, chemical, or pathogen-associated
    agents that impair translation may lead to IL-1ß-dependent inflammation through
    activation of the NLRP3 inflammasome. For agents that inhibit translation through
    decreased cellular potassium, the application of high extracellular potassium
    restores protein translation and suppresses activation of the NLRP inflammasome.
    For agents that inhibit translation through mechanisms that do not involve loss
    of potassium, high extracellular potassium suppresses IL-1ß processing through
    a mechanism that remains undefined.'
acknowledgement: "Supported by National Institutes of Health grants GM071338 (ML)
  and AI059355 (BM).\r\nWe acknowledge the expertise of Dr. Martina Ralle in Department
  of Biochemistry and Molecular Biology at OHSU for measurements of potassium using
  inductively coupled plasma mass spectrometry."
article_number: e36044
author:
- first_name: Meghan
  full_name: Vyleta, Meghan
  id: 418901AA-F248-11E8-B48F-1D18A9856A87
  last_name: Vyleta
- first_name: John
  full_name: Wong, John
  last_name: Wong
- first_name: Bruce
  full_name: Magun, Bruce
  last_name: Magun
citation:
  ama: Vyleta M, Wong J, Magun B. Suppression of ribosomal function triggers innate
    immune signaling through activation of the NLRP3 inflammasome. <i>PLoS One</i>.
    2012;7(5). doi:<a href="https://doi.org/10.1371/journal.pone.0036044">10.1371/journal.pone.0036044</a>
  apa: Vyleta, M., Wong, J., &#38; Magun, B. (2012). Suppression of ribosomal function
    triggers innate immune signaling through activation of the NLRP3 inflammasome.
    <i>PLoS One</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pone.0036044">https://doi.org/10.1371/journal.pone.0036044</a>
  chicago: Vyleta, Meghan, John Wong, and Bruce Magun. “Suppression of Ribosomal Function
    Triggers Innate Immune Signaling through Activation of the NLRP3 Inflammasome.”
    <i>PLoS One</i>. Public Library of Science, 2012. <a href="https://doi.org/10.1371/journal.pone.0036044">https://doi.org/10.1371/journal.pone.0036044</a>.
  ieee: M. Vyleta, J. Wong, and B. Magun, “Suppression of ribosomal function triggers
    innate immune signaling through activation of the NLRP3 inflammasome,” <i>PLoS
    One</i>, vol. 7, no. 5. Public Library of Science, 2012.
  ista: Vyleta M, Wong J, Magun B. 2012. Suppression of ribosomal function triggers
    innate immune signaling through activation of the NLRP3 inflammasome. PLoS One.
    7(5), e36044.
  mla: Vyleta, Meghan, et al. “Suppression of Ribosomal Function Triggers Innate Immune
    Signaling through Activation of the NLRP3 Inflammasome.” <i>PLoS One</i>, vol.
    7, no. 5, e36044, Public Library of Science, 2012, doi:<a href="https://doi.org/10.1371/journal.pone.0036044">10.1371/journal.pone.0036044</a>.
  short: M. Vyleta, J. Wong, B. Magun, PLoS One 7 (2012).
date_created: 2018-12-11T12:01:45Z
date_published: 2012-05-14T00:00:00Z
date_updated: 2021-01-12T07:41:29Z
day: '14'
ddc:
- '610'
department:
- _id: SyCr
doi: 10.1371/journal.pone.0036044
file:
- access_level: open_access
  checksum: 30cef37e27eaa467f6571b3640282010
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:14:30Z
  date_updated: 2020-07-14T12:46:01Z
  file_id: '5082'
  file_name: IST-2012-97-v1+1_journal.pone.0036044.pdf
  file_size: 2984012
  relation: main_file
file_date_updated: 2020-07-14T12:46:01Z
has_accepted_license: '1'
intvolume: '         7'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '3526'
pubrep_id: '97'
quality_controlled: '1'
scopus_import: 1
status: public
title: Suppression of ribosomal function triggers innate immune signaling through
  activation of the NLRP3 inflammasome
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2012'
...
---
_id: '3242'
abstract:
- lang: eng
  text: Due to the omnipresent risk of epidemics, insect societies have evolved sophisticated
    disease defences at the individual and colony level. An intriguing yet little
    understood phenomenon is that social contact to pathogen-exposed individuals reduces
    susceptibility of previously naive nestmates to this pathogen. We tested whether
    such social immunisation in Lasius ants against the entomopathogenic fungus Metarhizium
    anisopliae is based on active upregulation of the immune system of nestmates following
    contact to an infectious individual or passive protection via transfer of immune
    effectors among group members—that is, active versus passive immunisation. We
    found no evidence for involvement of passive immunisation via transfer of antimicrobials
    among colony members. Instead, intensive allogrooming behaviour between naive
    and pathogen-exposed ants before fungal conidia firmly attached to their cuticle
    suggested passage of the pathogen from the exposed individuals to their nestmates.
    By tracing fluorescence-labelled conidia we indeed detected frequent pathogen
    transfer to the nestmates, where they caused low-level infections as revealed
    by growth of small numbers of fungal colony forming units from their dissected
    body content. These infections rarely led to death, but instead promoted an enhanced
    ability to inhibit fungal growth and an active upregulation of immune genes involved
    in antifungal defences (defensin and prophenoloxidase, PPO). Contrarily, there
    was no upregulation of the gene cathepsin L, which is associated with antibacterial
    and antiviral defences, and we found no increased antibacterial activity of nestmates
    of fungus-exposed ants. This indicates that social immunisation after fungal exposure
    is specific, similar to recent findings for individual-level immune priming in
    invertebrates. Epidemiological modeling further suggests that active social immunisation
    is adaptive, as it leads to faster elimination of the disease and lower death
    rates than passive immunisation. Interestingly, humans have also utilised the
    protective effect of low-level infections to fight smallpox by intentional transfer
    of low pathogen doses (“variolation” or “inoculation”).
acknowledgement: Funding for this project was obtained by the German Research Foundation
  DFG (http://www.dfg.de/en/index.jsp) as an Individual Research Grant (CR118/2-1
  to SC) and the European Research Council (http://erc.europa.eu/) in form of two
  ERC Starting Grants (ERC-2009-StG240371-SocialVaccines to SC and ERC-2010-StG259294-LatentCauses
  to FJT). In addition, the Junge Akademie (Young Academy of the Berlin-Brandenburg
  Academy of Sciences and Humanities and the National Academy of Sciences Leopoldina
  (http://www.diejungeakademie.de/english/i​ndex.html) funded this joint Antnet project
  of SC and FJT. The funders had no role in study design, data collection and analysis,
  decision to publish, or preparation of the manuscript.
article_number: e1001300
author:
- first_name: Matthias
  full_name: Konrad, Matthias
  id: 46528076-F248-11E8-B48F-1D18A9856A87
  last_name: Konrad
- first_name: Meghan
  full_name: Vyleta, Meghan
  id: 418901AA-F248-11E8-B48F-1D18A9856A87
  last_name: Vyleta
- first_name: Fabian
  full_name: Theis, Fabian
  last_name: Theis
- first_name: Miriam
  full_name: Stock, Miriam
  id: 42462816-F248-11E8-B48F-1D18A9856A87
  last_name: Stock
- first_name: Simon
  full_name: Tragust, Simon
  id: 35A7A418-F248-11E8-B48F-1D18A9856A87
  last_name: Tragust
- first_name: Martina
  full_name: Klatt, Martina
  id: E60F29C6-E9AE-11E9-AF6E-D190C7302F38
  last_name: Klatt
- first_name: Verena
  full_name: Drescher, Verena
  last_name: Drescher
- first_name: Carsten
  full_name: Marr, Carsten
  last_name: Marr
- first_name: Line V
  full_name: Ugelvig, Line V
  id: 3DC97C8E-F248-11E8-B48F-1D18A9856A87
  last_name: Ugelvig
  orcid: 0000-0003-1832-8883
- first_name: Sylvia
  full_name: Cremer, Sylvia
  id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87
  last_name: Cremer
  orcid: 0000-0002-2193-3868
citation:
  ama: Konrad M, Vyleta M, Theis F, et al. Social transfer of pathogenic fungus promotes
    active immunisation in ant colonies. <i>PLoS Biology</i>. 2012;10(4). doi:<a href="https://doi.org/10.1371/journal.pbio.1001300">10.1371/journal.pbio.1001300</a>
  apa: Konrad, M., Vyleta, M., Theis, F., Stock, M., Tragust, S., Klatt, M., … Cremer,
    S. (2012). Social transfer of pathogenic fungus promotes active immunisation in
    ant colonies. <i>PLoS Biology</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pbio.1001300">https://doi.org/10.1371/journal.pbio.1001300</a>
  chicago: Konrad, Matthias, Meghan Vyleta, Fabian Theis, Miriam Stock, Simon Tragust,
    Martina Klatt, Verena Drescher, Carsten Marr, Line V Ugelvig, and Sylvia Cremer.
    “Social Transfer of Pathogenic Fungus Promotes Active Immunisation in Ant Colonies.”
    <i>PLoS Biology</i>. Public Library of Science, 2012. <a href="https://doi.org/10.1371/journal.pbio.1001300">https://doi.org/10.1371/journal.pbio.1001300</a>.
  ieee: M. Konrad <i>et al.</i>, “Social transfer of pathogenic fungus promotes active
    immunisation in ant colonies,” <i>PLoS Biology</i>, vol. 10, no. 4. Public Library
    of Science, 2012.
  ista: Konrad M, Vyleta M, Theis F, Stock M, Tragust S, Klatt M, Drescher V, Marr
    C, Ugelvig LV, Cremer S. 2012. Social transfer of pathogenic fungus promotes active
    immunisation in ant colonies. PLoS Biology. 10(4), e1001300.
  mla: Konrad, Matthias, et al. “Social Transfer of Pathogenic Fungus Promotes Active
    Immunisation in Ant Colonies.” <i>PLoS Biology</i>, vol. 10, no. 4, e1001300,
    Public Library of Science, 2012, doi:<a href="https://doi.org/10.1371/journal.pbio.1001300">10.1371/journal.pbio.1001300</a>.
  short: M. Konrad, M. Vyleta, F. Theis, M. Stock, S. Tragust, M. Klatt, V. Drescher,
    C. Marr, L.V. Ugelvig, S. Cremer, PLoS Biology 10 (2012).
date_created: 2018-12-11T12:02:13Z
date_published: 2012-04-03T00:00:00Z
date_updated: 2023-02-23T14:07:11Z
day: '03'
ddc:
- '570'
- '579'
department:
- _id: SyCr
doi: 10.1371/journal.pbio.1001300
ec_funded: 1
file:
- access_level: open_access
  checksum: 4ebacefd9fbab5c68adf829124115fd1
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:08:28Z
  date_updated: 2020-07-14T12:46:04Z
  file_id: '4689'
  file_name: IST-2012-96-v1+1_journal.pbio.1001300.pdf
  file_size: 674228
  relation: main_file
file_date_updated: 2020-07-14T12:46:04Z
has_accepted_license: '1'
intvolume: '        10'
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
project:
- _id: 25DAF0B2-B435-11E9-9278-68D0E5697425
  grant_number: CR-118/3-1
  name: Host-Parasite Coevolution
- _id: 25DC711C-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '243071'
  name: 'Social Vaccination in Ant Colonies: from Individual Mechanisms to Society
    Effects'
- _id: 25E0E184-B435-11E9-9278-68D0E5697425
  name: Antnet
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '3434'
pubrep_id: '96'
quality_controlled: '1'
related_material:
  record:
  - id: '9755'
    relation: research_data
    status: public
scopus_import: 1
status: public
title: Social transfer of pathogenic fungus promotes active immunisation in ant colonies
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2012'
...
---
_id: '9755'
abstract:
- lang: eng
  text: Due to the omnipresent risk of epidemics, insect societies have evolved sophisticated
    disease defences at the individual and colony level. An intriguing yet little
    understood phenomenon is that social contact to pathogen-exposed individuals reduces
    susceptibility of previously naive nestmates to this pathogen. We tested whether
    such social immunisation in Lasius ants against the entomopathogenic fungus Metarhizium
    anisopliae is based on active upregulation of the immune system of nestmates following
    contact to an infectious individual or passive protection via transfer of immune
    effectors among group members—that is, active versus passive immunisation. We
    found no evidence for involvement of passive immunisation via transfer of antimicrobials
    among colony members. Instead, intensive allogrooming behaviour between naive
    and pathogen-exposed ants before fungal conidia firmly attached to their cuticle
    suggested passage of the pathogen from the exposed individuals to their nestmates.
    By tracing fluorescence-labelled conidia we indeed detected frequent pathogen
    transfer to the nestmates, where they caused low-level infections as revealed
    by growth of small numbers of fungal colony forming units from their dissected
    body content. These infections rarely led to death, but instead promoted an enhanced
    ability to inhibit fungal growth and an active upregulation of immune genes involved
    in antifungal defences (defensin and prophenoloxidase, PPO). Contrarily, there
    was no upregulation of the gene cathepsin L, which is associated with antibacterial
    and antiviral defences, and we found no increased antibacterial activity of nestmates
    of fungus-exposed ants. This indicates that social immunisation after fungal exposure
    is specific, similar to recent findings for individual-level immune priming in
    invertebrates. Epidemiological modeling further suggests that active social immunisation
    is adaptive, as it leads to faster elimination of the disease and lower death
    rates than passive immunisation. Interestingly, humans have also utilised the
    protective effect of low-level infections to fight smallpox by intentional transfer
    of low pathogen doses (“variolation” or “inoculation”).
article_processing_charge: No
author:
- first_name: Matthias
  full_name: Konrad, Matthias
  id: 46528076-F248-11E8-B48F-1D18A9856A87
  last_name: Konrad
- first_name: Meghan
  full_name: Vyleta, Meghan
  id: 418901AA-F248-11E8-B48F-1D18A9856A87
  last_name: Vyleta
- first_name: Fabian
  full_name: Theis, Fabian
  last_name: Theis
- first_name: Miriam
  full_name: Stock, Miriam
  id: 42462816-F248-11E8-B48F-1D18A9856A87
  last_name: Stock
- first_name: Martina
  full_name: Klatt, Martina
  id: E60F29C6-E9AE-11E9-AF6E-D190C7302F38
  last_name: Klatt
- first_name: Verena
  full_name: Drescher, Verena
  last_name: Drescher
- first_name: Carsten
  full_name: Marr, Carsten
  last_name: Marr
- first_name: Line V
  full_name: Ugelvig, Line V
  id: 3DC97C8E-F248-11E8-B48F-1D18A9856A87
  last_name: Ugelvig
  orcid: 0000-0003-1832-8883
- first_name: Sylvia
  full_name: Cremer, Sylvia
  id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87
  last_name: Cremer
  orcid: 0000-0002-2193-3868
citation:
  ama: 'Konrad M, Vyleta M, Theis F, et al. Data from: Social transfer of pathogenic
    fungus promotes active immunisation in ant colonies. 2012. doi:<a href="https://doi.org/10.5061/dryad.sv37s">10.5061/dryad.sv37s</a>'
  apa: 'Konrad, M., Vyleta, M., Theis, F., Stock, M., Klatt, M., Drescher, V., … Cremer,
    S. (2012). Data from: Social transfer of pathogenic fungus promotes active immunisation
    in ant colonies. Dryad. <a href="https://doi.org/10.5061/dryad.sv37s">https://doi.org/10.5061/dryad.sv37s</a>'
  chicago: 'Konrad, Matthias, Meghan Vyleta, Fabian Theis, Miriam Stock, Martina Klatt,
    Verena Drescher, Carsten Marr, Line V Ugelvig, and Sylvia Cremer. “Data from:
    Social Transfer of Pathogenic Fungus Promotes Active Immunisation in Ant Colonies.”
    Dryad, 2012. <a href="https://doi.org/10.5061/dryad.sv37s">https://doi.org/10.5061/dryad.sv37s</a>.'
  ieee: 'M. Konrad <i>et al.</i>, “Data from: Social transfer of pathogenic fungus
    promotes active immunisation in ant colonies.” Dryad, 2012.'
  ista: 'Konrad M, Vyleta M, Theis F, Stock M, Klatt M, Drescher V, Marr C, Ugelvig
    LV, Cremer S. 2012. Data from: Social transfer of pathogenic fungus promotes active
    immunisation in ant colonies, Dryad, <a href="https://doi.org/10.5061/dryad.sv37s">10.5061/dryad.sv37s</a>.'
  mla: 'Konrad, Matthias, et al. <i>Data from: Social Transfer of Pathogenic Fungus
    Promotes Active Immunisation in Ant Colonies</i>. Dryad, 2012, doi:<a href="https://doi.org/10.5061/dryad.sv37s">10.5061/dryad.sv37s</a>.'
  short: M. Konrad, M. Vyleta, F. Theis, M. Stock, M. Klatt, V. Drescher, C. Marr,
    L.V. Ugelvig, S. Cremer, (2012).
date_created: 2021-07-30T08:39:13Z
date_published: 2012-09-27T00:00:00Z
date_updated: 2023-02-23T11:18:41Z
day: '27'
department:
- _id: SyCr
doi: 10.5061/dryad.sv37s
main_file_link:
- open_access: '1'
  url: https://doi.org/10.5061/dryad.sv37s
month: '09'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
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    relation: used_in_publication
    status: public
status: public
title: 'Data from: Social transfer of pathogenic fungus promotes active immunisation
  in ant colonies'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2012'
...
