Open AccessLeishmania infection inhibits macrophage motility by altering F‐actin dynamics and the expression of adhesion complex proteins
Author(s) -
Menezes Juliana Perrone Bezerra,
Koushik Amrita,
Das Satarupa,
Guven Can,
Siegel Ariel,
LaranjeiraSilva Maria Fernanda,
Losert Wolfgang,
Andrews Norma W.
Publication year - 2017
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12668
Subject(s) - biology , paxillin , microbiology and biotechnology , motility , macrophage , focal adhesion , leishmania , podosome , actin , actin cytoskeleton , extracellular matrix , phosphorylation , cytoskeleton , cell , parasite hosting , biochemistry , in vitro , computer science , world wide web
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.