ArticleCellular microbiology2017
Leishmania infection inhibits macrophage motility by altering F-actin dynamics and the expression of adhesion complex proteins.
Article in Cellular microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanisms of Immune Evasion, Dissemination, and Persistence in Leishmania amazonensis Infection.Parasite immunology · 2026Review
- Investigation of Viscoelastic Properties of Macrophage Membrane-Cytoskeleton Induced by Gold Nanorods in Leishmania Infection.Nanomaterials (Basel, Switzerland) · 2025Article
- New insights into the life cycle, host cell tropism, and infection amplification ofInfection and immunity · 2025Review
- Article
- The Toxoplasma effector GRA28 promotes parasite dissemination by inducing dendritic cell-like migratory properties in infected macrophages.Cell host & microbe · 2022Article
- Article
- Identification of the Host Substratome ofFrontiers in cell and developmental biology · 2021Article
- Complement receptor 3 mediates ruffle-like, actin-rich aggregates during phagocytosis of Leishmania infantum metacyclics.Experimental parasitology · 2021Article
- Review
- Trypanosoma cruzi down-regulates mechanosensitive proteins in cardiomyocytes.Memorias do Instituto Oswaldo Cruz · 2019Article
- CD100/Sema4D Increases Macrophage Infection byFrontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Leishmania is an intracellular protozoan parasite that causes a broad spectrum of clinical manifestations, ranging from self-healing skin lesions to fatal visceralizing disease. As the host cells of choice for all species of Leishmania, macrophages are critical for the establishment of infections. How macrophages contribute to parasite homing to specific tissues and how parasites modulate macrophage function are still poorly understood. In this study, we show that Leishmania amazonensis infection inhibits macrophage roaming motility. The reduction in macrophage speed is not dependent on particle load or on factors released by infected macrophages. L. amazonensis-infected macrophages also show reduced directional migration in response to the chemokine MCP-1. We found that infected macrophages have lower levels of total paxillin, phosphorylated paxillin, and phosphorylated focal adhesion kinase when compared to noninfected macrophages, indicating abnormalities in the formation of signaling adhesion complexes that regulate motility. Analysis of the dynamics of actin polymerization at peripheral sites also revealed a markedly enhanced F-actin turnover frequency in L. amazonensis-infected macrophages. Thus, Leishmania infection inhibits macrophage motility by altering actin dynamics and impairing the expression of proteins that function in plasma membrane-extracellular matrix interactions.
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Registered trials
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.