C-Kit Ligand Promotes Mast Cell Infection by Toxoplasma gondii
Mohamed Bidria, Marc Contib, Naïma Hanounc, René Lai Kuend, Frédéric Fegera, Zacharie Taoufiqb, Michel Arocka, Dominique Mazier b, Ioannis Vouldoukis *, b
Identifiers and Pagination:Year: 2008
First Page: 43
Last Page: 50
Publisher Id: TOPARAJ-2-43
Article History:Received Date: 17/3/2008
Revision Received Date: 28/4/2008
Acceptance Date: 30/4/2008
Electronic publication date: 19/5/2008
Collection year: 2008
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Biological functions of mast cells include a functional role in innate immunity against parasitic infections. Here, we demonstrated that mast cells could also play a role in the anti-microbial defenses regulation and might participate as a parasite reservoir. We observed that Toxoplasma gondii infected massively in vitro mouse bone marrow derived mast cells (BMMC), a mucosal mast cell (MMC) phenotype, followed by substantial cell lysis. This induced release of β- hexosaminidase, but not of preformed or neosynthesized TNF-α. Culturing MMC in the presence of recombinant mouse stem cell factor (c-kit ligand) led to their maturation into connective tissue-like mast cells (CTMC), which T. gondii was able to adhere on and to infect more. T. gondii infection did not induce release of β-hexosaminidase and serotonin from BMMC. These results demonstrated that mast cells interact with T. gondii and are massively infected, especially after their maturation by c-kit ligand.