Evidence map›Paper›PMID 27088212›Full record

ArticlePLoS biology2016

How Many Parameters Does It Take to Describe Disease Tolerance?

Alexander Louie, Kyung Han Song, Alejandra Hotson, Ann Thomas Tate, David S Schneider

Erratum issuedAbstract read
In one paragraph

Article in PLoS biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed.

  1. Article
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  3. Parasite defense covaries with reproductive timing, not with resistance.bioRxiv : the preprint server for biology · 2026
    Article
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  11. Article
  12. Genetic Resistance of Bovines to Theileriosis.Animals : an open access journal from MDPI · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Western diet regulates immune status and the response to LPS-driven sepsis independent of diet-associated microbiome.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Alexander LouieDepartment of Microbiology and Immunology, Stanford University, Stanford, California, United States of America.
Kyung Han SongDepartment of Microbiology and Immunology, Stanford University, Stanford, California, United States of America.
Alejandra HotsonDepartment of Microbiology and Immunology, Stanford University, Stanford, California, United States of America.
Ann Thomas TateDepartment of Biology and Biochemistry, University of Houston, Houston, Texas, United States of America.
David S SchneiderDepartment of Microbiology and Immunology, Stanford University, Stanford, California, United States of America.

Funding

Mapping the road to recovery - Does the way we get better differ from the way weDP1AT007753 · NCCIH · STANFORD UNIVERSITY · PI SCHNEIDER, DAVID S. · 2012 to 2015
$3.1M
NCCIH NIH HHS 5DP1AT007753NCCIH NIH HHS DP1 AT007753NIAID NIH HHS T32AI0070290
6 · The paper itself

Abstract

The study of infectious disease has been aided by model organisms, which have helped to elucidate molecular mechanisms and contributed to the development of new treatments; however, the lack of a conceptual framework for unifying findings across models, combined with host variability, has impeded progress and translation. Here, we fill this gap with a simple graphical and mathematical framework to study disease tolerance, the dose response curve relating health to microbe load; this approach helped uncover parameters that were previously overlooked. Using a model experimental system in which we challenged Drosophila melanogaster with the pathogen Listeria monocytogenes, we tested this framework, finding that microbe growth, the immune response, and disease tolerance were all well represented by sigmoid models. As we altered the system by varying host or pathogen genetics, disease tolerance varied, as we would expect if it was indeed governed by parameters controlling the sensitivity of the system (the number of bacteria required to trigger a response) and maximal effect size according to a logistic equation. Though either the pathogen or host immune response or both together could theoretically be the proximal cause of pathology that killed the flies, we found that the pathogen, but not the immune response, drove damage in this model. With this new understanding of the circuitry controlling disease tolerance, we can now propose better ways of choosing, combining, and developing treatments.

Indexed as

DiseaseAnimalsDrosophila melanogasterHumansListeria monocytogenes

Identifiers

PMID27088212
PMCPMC4835111

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.