Phosphoinositide-3-kinase-dependent, MyD88-independent induction of CC-type chemokines characterizes the macrophage response to Toxoplasma gondii strains with high virulence.
Infect Immun
; 75(12): 5788-97, 2007 Dec.
Article
em En
| MEDLINE
| ID: mdl-17908814
ABSTRACT
Chemokines play an important role in inflammation and infection due to their ability to recruit cells of innate and adaptive immunity. Here we examined mouse macrophage chemokine responses during intracellular infections with high- and low-virulence Toxoplasma gondii strains. The high-virulence type I strain RH induced a large panel of CC-type chemokines, whereas responses elicited by strains PTG (type II) and M7741 (type III) were much weaker. Strikingly, the T. gondii-induced chemokine response occurred independently of signaling through the Toll-like receptor adaptor MyD88. Instead, production of chemokines during infection was heavily dependent upon phosphoinositide-3-kinase signaling pathways. Because infection with type I strains such as RH results in an uncontrolled proinflammatory cytokine response, we hypothesize that this virulence phenotype is a consequence of early strong induction of chemokines by type I, but not type II or III, Toxoplasma strains.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Toxoplasma
/
Toxoplasmose
/
Fosfatidilinositol 3-Quinases
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Quimiocinas CC
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Fator 88 de Diferenciação Mieloide
/
Macrófagos
Limite:
Animals
Idioma:
En
Revista:
Infect Immun
Ano de publicação:
2007
Tipo de documento:
Article
País de afiliação:
Estados Unidos