The Open Parasitology Journal
2008, 2 : 43-50Published online 2008 May 19. DOI: 10.2174/1874421400802010043
Publisher ID: TOPARAJ-2-43
RESEARCH ARTICLE
C-Kit Ligand Promotes Mast Cell Infection by
b NSERM UMR S511, Immunobiologie Cellulaire et Moléculaire des Infections Parasitaires, CHU Pitié- Salpêtriéré, Université Pierre et Marie Curie-Paris6, 75013 Paris, France
c INSERM U677, Biochimie Médicale, CHU Pitié-Salpêtriére, Université Pierre et Marie Curie-Paris6, 75013 Paris, France
d Electron Microscopy Department, Faculty of Pharmacy, 4, Avenue de l'Observatoire, 75006 Paris, France
* Address correspondence to this author at the INSERM UMR S511, Immunobiologie Cellulaire et Moléculaire des Infections Parasitaires, Universitéc Pierre et Marie Curie-Paris6, CHU-Pitié-Salpêtrière, 91 bd de l’Hôpital, 75013 Paris, France; Tel: 33(0)1407781 09; Fax: 33(0)145838858; E-mail: vouldouk@chups.jussieu.fr
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 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.