Evidence map›Paper›PMID 39181505›Full record

ArticleMolecular and biochemical parasitology2024

Using machine learning to dissect host kinases required for Leishmania internalization and development.

Ling Wei, Umaru Barrie, Gina M Aloisio, Francis T H Khuong, Nadia Arang, Arani Datta, Alexis Kaushansky, Dawn M Wetzel

Abstract read
In one paragraph

Article in Molecular and biochemical parasitology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Ling WeiCenter for Global Infectious Disease Research, Seattle Children's Research Institute, Seattle, WA 98109, United States.
Umaru BarrieMedical Scientist Training Program, UT Southwestern Medical Center, Dallas, TX 75390, United States; Department of Pediatrics, UT Southwestern Medical Center, Dallas, TX 75390, United States.
Gina M AloisioMedical Scientist Training Program, UT Southwestern Medical Center, Dallas, TX 75390, United States; Department of Pediatrics, UT Southwestern Medical Center, Dallas, TX 75390, United States.
Francis T H KhuongDepartment of Pediatrics, UT Southwestern Medical Center, Dallas, TX 75390, United States.
Nadia ArangCenter for Global Infectious Disease Research, Seattle Children's Research Institute, Seattle, WA 98109, United States.
Arani DattaDepartment of Pediatrics, UT Southwestern Medical Center, Dallas, TX 75390, United States.
Alexis KaushanskyCenter for Global Infectious Disease Research, Seattle Children's Research Institute, Seattle, WA 98109, United States; Department of Pediatrics, University of Washington, Seattle, WA 98105, United States; Department of Global Health, University of Washington, Seattle, WA 98105, United States. Electronic address: alexis.kaushansky@seattlechildrens.org.
Dawn M WetzelDepartment of Pediatrics, UT Southwestern Medical Center, Dallas, TX 75390, United States; Department of Biochemistry, UT Southwestern Medical Center, Dallas, TX 75390, United States. Electronic address: dawn.wetzel@utsouthwestern.edu.

Funding

TRAINING THE MD PHD IN THE HEALTH SCIENCE CENTERT32GM008014 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ZINN, ANDREW R. · 1985 to 2024
$21.1M
Perturbations of host cell signaling by a complex hepatotropic pathogenR01GM101183 · NIGMS · SEATTLE CHILDREN'S HOSPITAL · PI KAUSHANSKY, ALEXIS · 2013 to 2021
$3.6M
Targeting a New Therapy for TrypanosomatidsR01AI146349 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI WETZEL, DAWN MARIE · 2019 to 2023
$3.0M
Perturbations of host cell signaling by a complex hepatotropic pathogenR01AI177257 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI Alexis Kaushansky · 2023 to 2026
$2.6M
APCs in Chronic Heart RejectionR01AI047257 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI TURKA, LAURENCE A · 2001 to 2003
$1.1M
In Cell Analyzer 6000 for UTSW HTS CoreS10OD018005 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI POSNER, BRUCE ARTHUR · 2014 to 2014
$598k
Targeting Entry Pathways in LeishmaniasisK08AI103036 · NIAID · YALE UNIVERSITY · PI WETZEL, DAWN MARIE · 2013 to 2015
$397k
NIAID NIH HHS K08 AI103036NIAID NIH HHS R01 AI047257NIAID NIH HHS R01 AI146349NIAID NIH HHS R01 AI146349-S1NIAID NIH HHS R01 AI177257NIGMS NIH HHS R01 GM101183NIGMS NIH HHS T32 GM008014NIH HHS S10 OD018005
6 · The paper itself

Abstract

The Leishmania life cycle alternates between promastigotes, found in the sandfly, and amastigotes, found in mammals. When an infected sandfly bites a host, promastigotes are engulfed by phagocytes (i.e., neutrophils, dendritic cells, and macrophages) to establish infection. When these phagocytes die or break down, amastigotes must be re-internalized to survive within the acidic phagolysosome and establish disease. To define host kinase regulators of Leishmania promastigote and amastigote uptake and survival within macrophages, we performed an image-based kinase regression screen using a panel of 38 kinase inhibitors with unique yet overlapping kinase targets. We also targeted inert beads to complement receptor 3 (CR3) or Fcγ receptors (FcR) as controls by coating them with complement/C3bi or IgG respectively. Through this approach, we identified several putative host kinases that regulate receptor-mediated phagocytosis and/or the uptake of L. amazonensis. Findings included kinases previously implicated in Leishmania uptake (such as Src family kinases (SFK), Abl family kinases (ABL1/c-Abl, ABL2/Arg), and spleen tyrosine kinase (SYK)), but we also uncovered many novel kinases. Our methods also predicted host kinases necessary for promastigotes to convert to amastigotes or for amastigotes to survive within macrophages. Overall, our results suggest that the concerted action of multiple interconnected networks of host kinases are needed over the course of Leishmania infection, and that the kinases required for the parasite's life cycle may differ substantially depending on which receptors are bound and the life cycle stage that is internalized. In addition, using our screen, we identified kinases that appear to preferentially regulate the uptake of parasites over beads, indicating that the methods required for Leishmania to be internalized by macrophages may differ from generalized phagocytic mechanisms. Our findings are intended to be used as a hypothesis generation resource for the broader scientific community studying the roles of kinases in host-pathogen interactions.

Indexed as

Machine LearningMacrophagesPhagocytosisAnimalsHost-Parasite InteractionsHumansLeishmaniaLeishmania mexicanaLeishmaniasisMiceProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablReceptors, IgGsrc-Family KinasesARG tyrosine kinaseProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablReceptors, IgGsrc-Family KinasesComplement receptorFc receptorKinase regressionLeishmaniaPhagocytosisPhosphosignaling

Identifiers

PMID39181505
PMCPMC12399033

What Socratic holds

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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 Socratic graph.