Fasciola hepatica tegumental antigens indirectly induce an M2 macrophage‐like phenotype in vivo. (October 2014)

• Record Type: Journal Article
• Authors: Adams, P. N.; Aldridge, A.; Vukman, K. V.; Donnelly, S.; O'Neill, S. M.
• Is Part Of: Parasite immunology. Volume 36:Number 10(2014:Oct.)
• Page Start: 531
• Page End: 539
• Publication Date: 2014-10
• Subjects: Veterinary parasitology -- Immunological aspects -- Periodicals; Host-parasite relationships -- Immunological aspects -- Periodicals; 571.96
• DOI: 10.1111/pim.12127
• Languages: English
• ISSNs: 0141-9838

Abstract

<abstract abstract-type="main" id="pim12127-abs-0001"> <title>Summary</title> <p>The M2 subset of macrophages has a critical role to play in host tissue repair, tissue fibrosis and modulation of adaptive immunity during helminth infection. Infection with the helminth, <italic>Fasciola hepatica, </italic> is associated with M2 macrophages in its mammalian host, and this response is mimicked by its excretory‐secretory products (FhES). The tegumental coat of <italic>F. hepatica</italic> (FhTeg) is another major source of immune‐modulatory molecules; we have previously shown that FhTeg can modulate the activity of both dendritic cells and mast cells inhibiting their ability to prime a Th1 immune response. Here, we report that FhTeg does not induce Th2 immune responses but can induce M2‐like phenotype <italic>in vivo</italic> that modulates cytokine production from CD4<sup>+</sup> cells in response to anti‐CD3 stimulation. FhTeg induces a RELMα expressing macrophage population <italic>in vitro, </italic> while <italic>in vivo, </italic> the expression of Arg1 and Ym‐1/2 but not RELMα in FhTeg‐stimulated macrophages was STAT6 dependent. To support this finding, FhTeg induces RELMα expression <italic>in vivo</italic> prior to the induction of IL‐13. FhTeg can induce IL‐13‐producing peritoneal macrophages following intraperitoneal injection This study highlights the important role of FhTeg as an immune‐modulatory source during <italic>F. hepatica</italic> infection and sheds further light on helminth–macrophage interactions.</p> </abstract>