---
_id: '7513'
abstract:
- lang: eng
  text: 'Social insects (i.e., ants, termites and the social bees and wasps) protect
    their colonies from disease using a combination of individual immunity and collectively
    performed defenses, termed social immunity. The first line of social immune defense
    is sanitary care, which is performed by colony members to protect their pathogen-exposed
    nestmates from developing an infection. If sanitary care fails and an infection
    becomes established, a second line of social immune defense is deployed to stop
    disease transmission within the colony and to protect the valuable queens, which
    together with the males are the reproductive individuals of the colony. Insect
    colonies are separated into these reproductive individuals and the sterile worker
    force, forming a superorganismal reproductive unit reminiscent of the differentiated
    germline and soma in a multicellular organism. Ultimately, the social immune response
    preserves the germline of the superorganism insect colony and increases overall
    fitness of the colony in case of disease. '
article_processing_charge: No
author:
- first_name: Sylvia
  full_name: Cremer, Sylvia
  id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87
  last_name: Cremer
  orcid: 0000-0002-2193-3868
- first_name: Megan
  full_name: Kutzer, Megan
  id: 29D0B332-F248-11E8-B48F-1D18A9856A87
  last_name: Kutzer
  orcid: 0000-0002-8696-6978
citation:
  ama: 'Cremer S, Kutzer M. Social immunity. In: Choe J, ed. <i>Encyclopedia of Animal
    Behavior</i>. 2nd ed. Elsevier; 2019:747-755. doi:<a href="https://doi.org/10.1016/B978-0-12-809633-8.90721-0">10.1016/B978-0-12-809633-8.90721-0</a>'
  apa: Cremer, S., &#38; Kutzer, M. (2019). Social immunity. In J. Choe (Ed.), <i>Encyclopedia
    of Animal Behavior</i> (2nd ed., pp. 747–755). Elsevier. <a href="https://doi.org/10.1016/B978-0-12-809633-8.90721-0">https://doi.org/10.1016/B978-0-12-809633-8.90721-0</a>
  chicago: Cremer, Sylvia, and Megan Kutzer. “Social Immunity.” In <i>Encyclopedia
    of Animal Behavior</i>, edited by Jae Choe, 2nd ed., 747–55. Elsevier, 2019. <a
    href="https://doi.org/10.1016/B978-0-12-809633-8.90721-0">https://doi.org/10.1016/B978-0-12-809633-8.90721-0</a>.
  ieee: S. Cremer and M. Kutzer, “Social immunity,” in <i>Encyclopedia of Animal Behavior</i>,
    2nd ed., J. Choe, Ed. Elsevier, 2019, pp. 747–755.
  ista: 'Cremer S, Kutzer M. 2019.Social immunity. In: Encyclopedia of Animal Behavior.
    , 747–755.'
  mla: Cremer, Sylvia, and Megan Kutzer. “Social Immunity.” <i>Encyclopedia of Animal
    Behavior</i>, edited by Jae Choe, 2nd ed., Elsevier, 2019, pp. 747–55, doi:<a
    href="https://doi.org/10.1016/B978-0-12-809633-8.90721-0">10.1016/B978-0-12-809633-8.90721-0</a>.
  short: S. Cremer, M. Kutzer, in:, J. Choe (Ed.), Encyclopedia of Animal Behavior,
    2nd ed., Elsevier, 2019, pp. 747–755.
date_created: 2020-02-23T23:00:36Z
date_published: 2019-02-06T00:00:00Z
date_updated: 2023-09-08T11:12:04Z
day: '06'
department:
- _id: SyCr
doi: 10.1016/B978-0-12-809633-8.90721-0
edition: '2'
editor:
- first_name: Jae
  full_name: Choe, Jae
  last_name: Choe
external_id:
  isi:
  - '000248989500026'
isi: 1
language:
- iso: eng
month: '02'
oa_version: None
page: 747-755
publication: Encyclopedia of Animal Behavior
publication_identifier:
  eisbn:
  - '9780128132524'
  isbn:
  - '9780128132517'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Social immunity
type: book_chapter
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '6105'
abstract:
- lang: eng
  text: "    Hosts can alter their strategy towards pathogens during their lifetime;
    that is, they can show phenotypic plasticity in immunity or life history. Immune
    priming is one such example, where a previous encounter with a pathogen confers
    enhanced protection upon secondary challenge, resulting in reduced pathogen load
    (i.e., resistance) and improved host survival. However, an initial encounter might
    also enhance tolerance, particularly to less virulent opportunistic pathogens
    that establish persistent infections. In this scenario, individuals are better
    able to reduce the negative fecundity consequences that result from a high pathogen
    burden. Finally, previous exposure may also lead to life‐history adjustments,
    such as terminal investment into reproduction.\r\n    Using different Drosophila
    melanogaster host genotypes and two bacterial pathogens, Lactococcus lactis and
    Pseudomonas entomophila, we tested whether previous exposure results in resistance
    or tolerance and whether it modifies immune gene expression during an acute‐phase
    infection (one day post‐challenge). We then asked whether previous pathogen exposure
    affects chronic‐phase pathogen persistence and longer‐term survival (28 days post‐challenge).\r\n
    \   We predicted that previous exposure would increase host resistance to an early
    stage bacterial infection while it might come at a cost to host fecundity tolerance.
    We reasoned that resistance would be due in part to stronger immune gene expression
    after challenge. We expected that previous exposure would improve long‐term survival,
    that it would reduce infection persistence, and we expected to find genetic variation
    in these responses.\r\n    We found that previous exposure to P. entomophila weakened
    host resistance to a second infection independent of genotype and had no effect
    on immune gene expression. Fecundity tolerance showed genotypic variation but
    was not influenced by previous exposure. However, L. lactis persisted as a chronic
    infection, whereas survivors cleared the more pathogenic P. entomophila infection.\r\n
    \   To our knowledge, this is the first study that addresses host tolerance to
    bacteria in relation to previous exposure, taking a multi‐faceted approach to
    address the topic. Our results suggest that previous exposure comes with transient
    costs to resistance during the early stage of infection in this host–pathogen
    system and that infection persistence may be bacterium‐specific.\r\n"
article_processing_charge: No
article_type: original
author:
- first_name: Megan
  full_name: Kutzer, Megan
  id: 29D0B332-F248-11E8-B48F-1D18A9856A87
  last_name: Kutzer
  orcid: 0000-0002-8696-6978
- first_name: Joachim
  full_name: Kurtz, Joachim
  last_name: Kurtz
- first_name: Sophie A.O.
  full_name: Armitage, Sophie A.O.
  last_name: Armitage
citation:
  ama: Kutzer M, Kurtz J, Armitage SAO. A multi-faceted approach testing the effects
    of previous bacterial exposure on resistance and tolerance. <i>Journal of Animal
    Ecology</i>. 2019;88(4):566-578. doi:<a href="https://doi.org/10.1111/1365-2656.12953">10.1111/1365-2656.12953</a>
  apa: Kutzer, M., Kurtz, J., &#38; Armitage, S. A. O. (2019). A multi-faceted approach
    testing the effects of previous bacterial exposure on resistance and tolerance.
    <i>Journal of Animal Ecology</i>. Wiley. <a href="https://doi.org/10.1111/1365-2656.12953">https://doi.org/10.1111/1365-2656.12953</a>
  chicago: Kutzer, Megan, Joachim Kurtz, and Sophie A.O. Armitage. “A Multi-Faceted
    Approach Testing the Effects of Previous Bacterial Exposure on Resistance and
    Tolerance.” <i>Journal of Animal Ecology</i>. Wiley, 2019. <a href="https://doi.org/10.1111/1365-2656.12953">https://doi.org/10.1111/1365-2656.12953</a>.
  ieee: M. Kutzer, J. Kurtz, and S. A. O. Armitage, “A multi-faceted approach testing
    the effects of previous bacterial exposure on resistance and tolerance,” <i>Journal
    of Animal Ecology</i>, vol. 88, no. 4. Wiley, pp. 566–578, 2019.
  ista: Kutzer M, Kurtz J, Armitage SAO. 2019. A multi-faceted approach testing the
    effects of previous bacterial exposure on resistance and tolerance. Journal of
    Animal Ecology. 88(4), 566–578.
  mla: Kutzer, Megan, et al. “A Multi-Faceted Approach Testing the Effects of Previous
    Bacterial Exposure on Resistance and Tolerance.” <i>Journal of Animal Ecology</i>,
    vol. 88, no. 4, Wiley, 2019, pp. 566–78, doi:<a href="https://doi.org/10.1111/1365-2656.12953">10.1111/1365-2656.12953</a>.
  short: M. Kutzer, J. Kurtz, S.A.O. Armitage, Journal of Animal Ecology 88 (2019)
    566–578.
date_created: 2019-03-17T22:59:15Z
date_published: 2019-04-01T00:00:00Z
date_updated: 2023-08-25T08:04:53Z
day: '01'
ddc:
- '570'
department:
- _id: SyCr
doi: 10.1111/1365-2656.12953
ec_funded: 1
external_id:
  isi:
  - '000467994800007'
file:
- access_level: open_access
  checksum: 405cde15120de26018b3bd0dfa29986c
  content_type: application/pdf
  creator: dernst
  date_created: 2019-03-18T07:43:06Z
  date_updated: 2020-07-14T12:47:19Z
  file_id: '6107'
  file_name: 2019_JournalAnimalEcology_Kutzer.pdf
  file_size: 1460662
  relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: '        88'
isi: 1
issue: '4'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '04'
oa: 1
oa_version: Published Version
page: 566-578
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Journal of Animal Ecology
publication_identifier:
  eissn:
  - '13652656'
  issn:
  - '00218790'
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
  record:
  - id: '9806'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: A multi-faceted approach testing the effects of previous bacterial exposure
  on resistance and tolerance
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 88
year: '2019'
...
---
_id: '9806'
abstract:
- lang: eng
  text: 1. Hosts can alter their strategy towards pathogens during their lifetime,
    i.e., they can show phenotypic plasticity in immunity or life history. Immune
    priming is one such example, where a previous encounter with a pathogen confers
    enhanced protection upon secondary challenge, resulting in reduced pathogen load
    (i.e. resistance) and improved host survival. However, an initial encounter might
    also enhance tolerance, particularly to less virulent opportunistic pathogens
    that establish persistent infections. In this scenario, individuals are better
    able to reduce the negative fitness consequences that result from a high pathogen
    load. Finally, previous exposure may also lead to life history adjustments, such
    as terminal investment into reproduction. 2. Using different Drosophila melanogaster
    host genotypes and two bacterial pathogens, Lactococcus lactis and Pseudomonas
    entomophila, we tested if previous exposure results in resistance or tolerance
    and whether it modifies immune gene expression during an acute-phase infection
    (one day post-challenge). We then asked if previous pathogen exposure affects
    chronic-phase pathogen persistence and longer-term survival (28 days post-challenge).
    3. We predicted that previous exposure would increase host resistance to an early
    stage bacterial infection while it might come at a cost to host fecundity tolerance.
    We reasoned that resistance would be due in part to stronger immune gene expression
    after challenge. We expected that previous exposure would improve long-term survival,
    that it would reduce infection persistence, and we expected to find genetic variation
    in these responses. 4. We found that previous exposure to P. entomophila weakened
    host resistance to a second infection independent of genotype and had no effect
    on immune gene expression. Fecundity tolerance showed genotypic variation but
    was not influenced by previous exposure. However, L. lactis persisted as a chronic
    infection, whereas survivors cleared the more pathogenic P. entomophila infection.
    5. To our knowledge, this is the first study that addresses host tolerance to
    bacteria in relation to previous exposure, taking a multi-faceted approach to
    address the topic. Our results suggest that previous exposure comes with transient
    costs to resistance during the early stage of infection in this host-pathogen
    system and that infection persistence may be bacterium-specific.
article_processing_charge: No
author:
- first_name: Megan
  full_name: Kutzer, Megan
  id: 29D0B332-F248-11E8-B48F-1D18A9856A87
  last_name: Kutzer
  orcid: 0000-0002-8696-6978
- first_name: Joachim
  full_name: Kurtz, Joachim
  last_name: Kurtz
- first_name: Sophie A.O.
  full_name: Armitage, Sophie A.O.
  last_name: Armitage
citation:
  ama: 'Kutzer M, Kurtz J, Armitage SAO. Data from: A multi-faceted approach testing
    the effects of previous bacterial exposure on resistance and tolerance. 2019.
    doi:<a href="https://doi.org/10.5061/dryad.9kj41f0">10.5061/dryad.9kj41f0</a>'
  apa: 'Kutzer, M., Kurtz, J., &#38; Armitage, S. A. O. (2019). Data from: A multi-faceted
    approach testing the effects of previous bacterial exposure on resistance and
    tolerance. Dryad. <a href="https://doi.org/10.5061/dryad.9kj41f0">https://doi.org/10.5061/dryad.9kj41f0</a>'
  chicago: 'Kutzer, Megan, Joachim Kurtz, and Sophie A.O. Armitage. “Data from: A
    Multi-Faceted Approach Testing the Effects of Previous Bacterial Exposure on Resistance
    and Tolerance.” Dryad, 2019. <a href="https://doi.org/10.5061/dryad.9kj41f0">https://doi.org/10.5061/dryad.9kj41f0</a>.'
  ieee: 'M. Kutzer, J. Kurtz, and S. A. O. Armitage, “Data from: A multi-faceted approach
    testing the effects of previous bacterial exposure on resistance and tolerance.”
    Dryad, 2019.'
  ista: 'Kutzer M, Kurtz J, Armitage SAO. 2019. Data from: A multi-faceted approach
    testing the effects of previous bacterial exposure on resistance and tolerance,
    Dryad, <a href="https://doi.org/10.5061/dryad.9kj41f0">10.5061/dryad.9kj41f0</a>.'
  mla: 'Kutzer, Megan, et al. <i>Data from: A Multi-Faceted Approach Testing the Effects
    of Previous Bacterial Exposure on Resistance and Tolerance</i>. Dryad, 2019, doi:<a
    href="https://doi.org/10.5061/dryad.9kj41f0">10.5061/dryad.9kj41f0</a>.'
  short: M. Kutzer, J. Kurtz, S.A.O. Armitage, (2019).
date_created: 2021-08-06T12:06:40Z
date_published: 2019-02-05T00:00:00Z
date_updated: 2023-08-25T08:04:52Z
day: '05'
department:
- _id: SyCr
doi: 10.5061/dryad.9kj41f0
main_file_link:
- open_access: '1'
  url: https://doi.org/10.5061/dryad.9kj41f0
month: '02'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
  record:
  - id: '6105'
    relation: used_in_publication
    status: public
status: public
title: 'Data from: A multi-faceted approach testing the effects of previous bacterial
  exposure on resistance and tolerance'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2019'
...
---
_id: '617'
abstract:
- lang: eng
  text: Insects are exposed to a variety of potential pathogens in their environment,
    many of which can severely impact fitness and health. Consequently, hosts have
    evolved resistance and tolerance strategies to suppress or cope with infections.
    Hosts utilizing resistance improve fitness by clearing or reducing pathogen loads,
    and hosts utilizing tolerance reduce harmful fitness effects per pathogen load.
    To understand variation in, and selective pressures on, resistance and tolerance,
    we asked to what degree they are shaped by host genetic background, whether plasticity
    in these responses depends upon dietary environment, and whether there are interactions
    between these two factors. Females from ten wild-type Drosophila melanogaster
    genotypes were kept on high- or low-protein (yeast) diets and infected with one
    of two opportunistic bacterial pathogens, Lactococcus lactis or Pseudomonas entomophila.
    We measured host resistance as the inverse of bacterial load in the early infection
    phase. The relationship (slope) between fly fecundity and individual-level bacteria
    load provided our fecundity tolerance measure. Genotype and dietary yeast determined
    host fecundity and strongly affected survival after infection with pathogenic
    P. entomophila. There was considerable genetic variation in host resistance, a
    commonly found phenomenon resulting from for example varying resistance costs
    or frequency-dependent selection. Despite this variation and the reproductive
    cost of higher P. entomophila loads, fecundity tolerance did not vary across genotypes.
    The absence of genetic variation in tolerance may suggest that at this early infection
    stage, fecundity tolerance is fixed or that any evolved tolerance mechanisms are
    not expressed under these infection conditions.
acknowledgement: 'We would like to thank Susann Wicke for performing the genome-wide
  SNP/indel analyses, as well as Veronica Alves, Kevin Ferro, Momir Futo, Barbara
  Hasert, Dafne Maximo, Nora Schulz, Marlene Sroka, and Barth Wieczorek for technical
  help. We thank Brian Lazzaro for the L. lactis strain and Bruno Lemaitre for the
  Pseudomonas entomophila strain. We would like to thank two anonymous reviewers for
  their helpful comments. We are grateful to the Deutsche Forschungsgemeinschaft (DFG)
  priority programme 1399 ‘Host parasite coevolution’ for funding this project (AR
  872/1-1). '
article_processing_charge: No
article_type: original
author:
- first_name: Megan
  full_name: Kutzer, Megan
  id: 29D0B332-F248-11E8-B48F-1D18A9856A87
  last_name: Kutzer
  orcid: 0000-0002-8696-6978
- first_name: Joachim
  full_name: Kurtz, Joachim
  last_name: Kurtz
- first_name: Sophie
  full_name: Armitage, Sophie
  last_name: Armitage
citation:
  ama: Kutzer M, Kurtz J, Armitage S. Genotype and diet affect resistance, survival,
    and fecundity but not fecundity tolerance. <i>Journal of Evolutionary Biology</i>.
    2018;31(1):159-171. doi:<a href="https://doi.org/10.1111/jeb.13211">10.1111/jeb.13211</a>
  apa: Kutzer, M., Kurtz, J., &#38; Armitage, S. (2018). Genotype and diet affect
    resistance, survival, and fecundity but not fecundity tolerance. <i>Journal of
    Evolutionary Biology</i>. Wiley. <a href="https://doi.org/10.1111/jeb.13211">https://doi.org/10.1111/jeb.13211</a>
  chicago: Kutzer, Megan, Joachim Kurtz, and Sophie Armitage. “Genotype and Diet Affect
    Resistance, Survival, and Fecundity but Not Fecundity Tolerance.” <i>Journal of
    Evolutionary Biology</i>. Wiley, 2018. <a href="https://doi.org/10.1111/jeb.13211">https://doi.org/10.1111/jeb.13211</a>.
  ieee: M. Kutzer, J. Kurtz, and S. Armitage, “Genotype and diet affect resistance,
    survival, and fecundity but not fecundity tolerance,” <i>Journal of Evolutionary
    Biology</i>, vol. 31, no. 1. Wiley, pp. 159–171, 2018.
  ista: Kutzer M, Kurtz J, Armitage S. 2018. Genotype and diet affect resistance,
    survival, and fecundity but not fecundity tolerance. Journal of Evolutionary Biology.
    31(1), 159–171.
  mla: Kutzer, Megan, et al. “Genotype and Diet Affect Resistance, Survival, and Fecundity
    but Not Fecundity Tolerance.” <i>Journal of Evolutionary Biology</i>, vol. 31,
    no. 1, Wiley, 2018, pp. 159–71, doi:<a href="https://doi.org/10.1111/jeb.13211">10.1111/jeb.13211</a>.
  short: M. Kutzer, J. Kurtz, S. Armitage, Journal of Evolutionary Biology 31 (2018)
    159–171.
date_created: 2018-12-11T11:47:31Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2023-09-11T14:06:04Z
day: '01'
department:
- _id: SyCr
doi: 10.1111/jeb.13211
external_id:
  isi:
  - '000419307000014'
  pmid:
  - '29150962'
intvolume: '        31'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1111/jeb.13211
month: '01'
oa: 1
oa_version: Published Version
page: 159  - 171
pmid: 1
publication: Journal of Evolutionary Biology
publication_identifier:
  eissn:
  - 1420-9101
  issn:
  - 1010-061X
publication_status: published
publisher: Wiley
publist_id: '7187'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Genotype and diet affect resistance, survival, and fecundity but not fecundity
  tolerance
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 31
year: '2018'
...
---
_id: '558'
abstract:
- lang: eng
  text: Immune specificity is the degree to which a host’s immune system discriminates
    among various pathogens or antigenic variants. Vertebrate immune memory is highly
    specific due to antibody responses. On the other hand, some invertebrates show
    immune priming, i.e. improved survival after secondary exposure to a previously
    encountered pathogen. Until now, specificity of priming has only been demonstrated
    via the septic infection route or when live pathogens were used for priming. Therefore,
    we tested for specificity in the oral priming route in the red flour beetle, Tribolium
    castaneum. For priming, we used pathogen-free supernatants derived from three
    different strains of the entomopathogen, Bacillus thuringiensis, which express
    different Cry toxin variants known for their toxicity against this beetle. Subsequent
    exposure to the infective spores showed that oral priming was specific for two
    naturally occurring strains, while a third engineered strain did not induce any
    priming effect. Our data demonstrate that oral immune priming with a non-infectious
    bacterial agent can be specific, but the priming effect is not universal across
    all bacterial strains.
article_number: '0632'
article_processing_charge: No
article_type: original
author:
- first_name: Momir
  full_name: Futo, Momir
  last_name: Futo
- first_name: Marie
  full_name: Sell, Marie
  last_name: Sell
- first_name: Megan
  full_name: Kutzer, Megan
  id: 29D0B332-F248-11E8-B48F-1D18A9856A87
  last_name: Kutzer
  orcid: 0000-0002-8696-6978
- first_name: Joachim
  full_name: Kurtz, Joachim
  last_name: Kurtz
citation:
  ama: Futo M, Sell M, Kutzer M, Kurtz J. Specificity of oral immune priming in the
    red flour beetle Tribolium castaneum. <i>Biology Letters</i>. 2017;13(12). doi:<a
    href="https://doi.org/10.1098/rsbl.2017.0632">10.1098/rsbl.2017.0632</a>
  apa: Futo, M., Sell, M., Kutzer, M., &#38; Kurtz, J. (2017). Specificity of oral
    immune priming in the red flour beetle Tribolium castaneum. <i>Biology Letters</i>.
    The Royal Society. <a href="https://doi.org/10.1098/rsbl.2017.0632">https://doi.org/10.1098/rsbl.2017.0632</a>
  chicago: Futo, Momir, Marie Sell, Megan Kutzer, and Joachim Kurtz. “Specificity
    of Oral Immune Priming in the Red Flour Beetle Tribolium Castaneum.” <i>Biology
    Letters</i>. The Royal Society, 2017. <a href="https://doi.org/10.1098/rsbl.2017.0632">https://doi.org/10.1098/rsbl.2017.0632</a>.
  ieee: M. Futo, M. Sell, M. Kutzer, and J. Kurtz, “Specificity of oral immune priming
    in the red flour beetle Tribolium castaneum,” <i>Biology Letters</i>, vol. 13,
    no. 12. The Royal Society, 2017.
  ista: Futo M, Sell M, Kutzer M, Kurtz J. 2017. Specificity of oral immune priming
    in the red flour beetle Tribolium castaneum. Biology Letters. 13(12), 0632.
  mla: Futo, Momir, et al. “Specificity of Oral Immune Priming in the Red Flour Beetle
    Tribolium Castaneum.” <i>Biology Letters</i>, vol. 13, no. 12, 0632, The Royal
    Society, 2017, doi:<a href="https://doi.org/10.1098/rsbl.2017.0632">10.1098/rsbl.2017.0632</a>.
  short: M. Futo, M. Sell, M. Kutzer, J. Kurtz, Biology Letters 13 (2017).
date_created: 2018-12-11T11:47:10Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2023-10-18T06:42:25Z
day: '01'
department:
- _id: SyCr
doi: 10.1098/rsbl.2017.0632
external_id:
  pmid:
  - '29237813'
intvolume: '        13'
issue: '12'
language:
- iso: eng
month: '12'
oa_version: None
pmid: 1
publication: Biology Letters
publication_identifier:
  issn:
  - 1744-9561
publication_status: published
publisher: The Royal Society
publist_id: '7255'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Specificity of oral immune priming in the red flour beetle Tribolium castaneum
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2017'
...
---
_id: '618'
abstract:
- lang: eng
  text: 'Background: Increasing temperatures are predicted to strongly impact host-parasite
    interactions, but empirical tests are rare. Host species that are naturally exposed
    to a broad temperature spectrum offer the possibility to investigate the effects
    of elevated temperatures on hosts and parasites. Using three-spined sticklebacks,
    Gasterosteus aculeatus L., and tapeworms, Schistocephalus solidus (Müller, 1776),
    originating from a cold and a warm water site of a volcanic lake, we subjected
    sympatric and allopatric host-parasite combinations to cold and warm conditions
    in a fully crossed design. We predicted that warm temperatures would promote the
    development of the parasites, while the hosts might benefit from cooler temperatures.
    We further expected adaptations to the local temperature and mutual adaptations
    of local host-parasite pairs. Results: Overall, S. solidus parasites grew faster
    at warm temperatures and stickleback hosts at cold temperatures. On a finer scale,
    we observed that parasites were able to exploit their hosts more efficiently at
    the parasite’s temperature of origin. In contrast, host tolerance towards parasite
    infection was higher when sticklebacks were infected with parasites at the parasite’s
    ‘foreign’ temperature. Cold-origin sticklebacks tended to grow faster and parasite
    infection induced a stronger immune response. Conclusions: Our results suggest
    that increasing environmental temperatures promote the parasite rather than the
    host and that host tolerance is dependent on the interaction between parasite
    infection and temperature. Sticklebacks might use tolerance mechanisms towards
    parasite infection in combination with their high plasticity towards temperature
    changes to cope with increasing parasite infection pressures and rising temperatures.'
article_number: '52'
author:
- first_name: Frederik
  full_name: Franke, Frederik
  last_name: Franke
- first_name: Sophie
  full_name: Armitage, Sophie
  last_name: Armitage
- first_name: Megan
  full_name: Kutzer, Megan
  id: 29D0B332-F248-11E8-B48F-1D18A9856A87
  last_name: Kutzer
  orcid: 0000-0002-8696-6978
- first_name: Joachim
  full_name: Kurtz, Joachim
  last_name: Kurtz
- first_name: Jörn
  full_name: Scharsack, Jörn
  last_name: Scharsack
citation:
  ama: Franke F, Armitage S, Kutzer M, Kurtz J, Scharsack J. Environmental temperature
    variation influences fitness trade-offs in a fish-tapeworm association . <i>Parasites
    &#38; Vectors</i>. 2017;10(252). doi:<a href="https://doi.org/10.1186/s13071-017-2192-7">10.1186/s13071-017-2192-7</a>
  apa: Franke, F., Armitage, S., Kutzer, M., Kurtz, J., &#38; Scharsack, J. (2017).
    Environmental temperature variation influences fitness trade-offs in a fish-tapeworm
    association . <i>Parasites &#38; Vectors</i>. BioMed Central. <a href="https://doi.org/10.1186/s13071-017-2192-7">https://doi.org/10.1186/s13071-017-2192-7</a>
  chicago: Franke, Frederik, Sophie Armitage, Megan Kutzer, Joachim Kurtz, and Jörn
    Scharsack. “Environmental Temperature Variation Influences Fitness Trade-Offs
    in a Fish-Tapeworm Association .” <i>Parasites &#38; Vectors</i>. BioMed Central,
    2017. <a href="https://doi.org/10.1186/s13071-017-2192-7">https://doi.org/10.1186/s13071-017-2192-7</a>.
  ieee: F. Franke, S. Armitage, M. Kutzer, J. Kurtz, and J. Scharsack, “Environmental
    temperature variation influences fitness trade-offs in a fish-tapeworm association
    ,” <i>Parasites &#38; Vectors</i>, vol. 10, no. 252. BioMed Central, 2017.
  ista: Franke F, Armitage S, Kutzer M, Kurtz J, Scharsack J. 2017. Environmental
    temperature variation influences fitness trade-offs in a fish-tapeworm association
    . Parasites &#38; Vectors. 10(252), 52.
  mla: Franke, Frederik, et al. “Environmental Temperature Variation Influences Fitness
    Trade-Offs in a Fish-Tapeworm Association .” <i>Parasites &#38; Vectors</i>, vol.
    10, no. 252, 52, BioMed Central, 2017, doi:<a href="https://doi.org/10.1186/s13071-017-2192-7">10.1186/s13071-017-2192-7</a>.
  short: F. Franke, S. Armitage, M. Kutzer, J. Kurtz, J. Scharsack, Parasites &#38;
    Vectors 10 (2017).
date_created: 2018-12-11T11:47:31Z
date_published: 2017-06-02T00:00:00Z
date_updated: 2021-01-12T08:06:35Z
day: '02'
ddc:
- '570'
doi: 10.1186/s13071-017-2192-7
extern: '1'
file:
- access_level: open_access
  checksum: 742943377a38ee208108705b8e2f4dbf
  content_type: application/pdf
  creator: dernst
  date_created: 2019-01-21T13:45:36Z
  date_updated: 2020-07-14T12:47:22Z
  file_id: '5864'
  file_name: 2017_Parasites_Franke.pdf
  file_size: 671807
  relation: main_file
file_date_updated: 2020-07-14T12:47:22Z
has_accepted_license: '1'
intvolume: '        10'
issue: '252'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Parasites & Vectors
publication_identifier:
  issn:
  - '17563305'
publication_status: published
publisher: BioMed Central
publist_id: '7186'
quality_controlled: '1'
status: public
title: 'Environmental temperature variation influences fitness trade-offs in a fish-tapeworm
  association '
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: '2017'
...
