Evidence map›Paper›PMID 28381313›Full record

ArticleComparative medicine2017

Influence of Genetic Background on Hematologic and Histopathologic Alterations during Acute Granulocytic Anaplasmosis in 129/SvEv and C57BL/6J Mice Lacking Type I and Type II Interferon Signaling.

Jennifer L Johns, Marielle L Discipulo, Amanda L Koehne, Kaitlin A Moorhead, Claude M Nagamine

Open access · greenAbstract readComparative Study
In one paragraph

Article in Comparative medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 44% of its field
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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Differential Susceptibility of Male Versus Female Laboratory Mice toTropical medicine and infectious disease · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Jennifer L JohnsDepartment of Biomedical Sciences, Oregon State University College of Veterinary Medicine, Corvallis, Oregon;, Email: jennifer.johns@oregonstate.edu.
Marielle L DiscipuloDepartments of Comparative Medicine, Stanford University School of Medicine, Stanford, California.
Amanda L KoehneDepartments of Pediatrics, Stanford University School of Medicine, Stanford, California.
Kaitlin A MoorheadDepartments of Comparative Medicine, Stanford University School of Medicine, Stanford, California.
Claude M NagamineDepartments of Comparative Medicine, Stanford University School of Medicine, Stanford, California.
Oregon State University · USStanford University · US

Funding

Dynamics of neutrophil trafficking in Granulocytic AnaplasmosisK01OD011150 · OD · STANFORD UNIVERSITY · PI JOHNS, JENNIFER LYNN · 2012 to 2015
$516k
NIH HHS K01 OD011150
6 · The paper itself

Abstract

The role of host type I IFN signaling and its interaction with other immune pathways during bacterial infections is incompletely understood. Type II IFN signaling plays a key role during numerous bacterial infections including granulocytic anaplasmosis (GA) caused by Anaplasma phagocytophilum infection. The function of combined type I and type II IFN signaling and their potential synergism during GA and similar tick-borne diseases is a topic of current research investigation. The goal of this study was to evaluate 2 mouse models of absent type I/type II IFN signaling in experimental A. phagocytophilum infection to determine the effects of background strain. Mice lacking both type I and type II IFN receptor signaling (IFNAR-/-/IFNGR-/-) on either the 129/SvEv or C57BL/6J genetic background were evaluated at days 0, 6, 8, and 12 of infection. Pathogen burden in multiple organs was largely similar between strains of infected mice, with few significant differences. Background strain influenced the immune response to infection. Mice of the 129/SvEv strain developed more severe hematologic abnormalities, particularly more severe leukocytosis with marked neutrophilia and lymphocytosis, throughout acute infection. Histopathologic changes occurred in infected mice of both strains and varied in severity by organ. 129/SvEv mice developed more severe pathologic changes in spleen and bone marrow, whereas C57BL/6J mice developed more severe renal pathology. This work highlights the importance of mouse background strain in dictating pathophysiologic response to infection and informs future work regarding the loss of type I and type II IFN signaling on the immune response during GA.

Indexed as

AnaplasmosisAnimalsDisease Models, AnimalGenetic Predisposition to DiseaseInterferon-gammaInterferon Type IMice, Inbred C57BLMice, Inbred StrainsParasite LoadSignal TransductionInterferon-gammaInterferon Type I

Identifiers

PMID28381313
PMCPMC5402732
OpenAlexW2981311461

What OpenQuestion holds

Textmetadata
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.