Nod1, but not the ASC inflammasome, contributes to induction of IL-1ß secretion in human trophoblasts after sensing of Chlamydia trachomatis.
Mucosal Immunol
; 6(2): 235-43, 2013 Mar.
Article
em En
| MEDLINE
| ID: mdl-22763410
ABSTRACT
Chlamydia trachomatis (Ct) is an obligate intracellular bacterial pathogen. Previously, we showed that infection of human trophoblast cells by Ct triggers the secretion of the pro-inflammatory cytokine, interleukin (IL)-1ß. The aim of this study was to understand the innate immune pathways involved in trophoblast production of IL-1ß after Ct infection. The approach we took was to inhibit the expression or function of the key Toll-like receptors (TLRs), Nod-like receptors, and inflammasome components that have been associated with chlamydia infection. In this study, we report that Ct-induced trophoblast IL-1ß secretion is associated with the transcription of IL-1ß mRNA, the translation and processing of pro-IL-1ß, and the activation of caspase-1. In addition, we demonstrate that Ct-induced IL-1ß production and secretion by the trophoblast is independent of TLR2, TLR4, MyD88, and the Nalp3/ASC inflammasome. Instead we report, for the first time, the importance of Nod1 for mediating trophoblast IL-1ß secretion in response to a Ct infection.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Trofoblastos
/
Chlamydia trachomatis
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Interleucina-1beta
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Proteína Adaptadora de Sinalização NOD1
Idioma:
En
Ano de publicação:
2013
Tipo de documento:
Article