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Abstract
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 partici- pate 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 - hexosaminidase, but not of preformed or neosynthesized TNF- . 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 -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.
Highlights
Cytokines derived from macrophages and T cells are known to play an important regulatory role in host defense and to control the susceptibility to microbial infection
We studied the interaction between mucosal mast cell (MMC) after their maturation into connective tissue-like cells (CTMC) and T. gondii
In less than 30 minutes, T. gondii parasites adhered to cultured mast cells
Summary
Cytokines derived from macrophages and T cells are known to play an important regulatory role in host defense and to control the susceptibility to microbial infection. IL-1, IL-6, IFN-, IL-12 and TNF- are involved in host protection against Toxoplasma gondii infection [1]. During T. gondii infection an important role for IFN- and TNF- has been proposed both in the development of the disease and the mobilization of efficient defense mechanisms [2,3,4,5]. Its attachment to the host cell is the first step required for the mechanism of invasion, and the second step is critical for its silent survival. The process for the identification of parasite ligands and cell surface receptors remains incomplete [6, 7]
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