Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis

• Published in: Mucosal immunology Vol. 6; no. 2; pp. 235 - 243
• Main Authors: Kavathas, P B, Boeras, C M, Mulla, M J, Abrahams, V M
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01-03-2013
• Subjects: 631/250/127/1213; 631/250/256/2177; 631/250/347; 692/699/255/1318; Allergology; Antibodies; Biomedical and Life Sciences; Biomedicine; CARD Signaling Adaptor Proteins; Carrier Proteins - metabolism; Cell Line; Chlamydia trachomatis - immunology; Cytoskeletal Proteins - metabolism; Gastroenterology; Gene Expression; Humans; Immunology; Inflammasomes - metabolism; Interleukin-1beta - genetics; Interleukin-1beta - metabolism; Myeloid Differentiation Factor 88 - metabolism; NLR Family, Pyrin Domain-Containing 3 Protein; Nod1 Signaling Adaptor Protein - metabolism; Toll-Like Receptor 2 - metabolism; Toll-Like Receptor 4 - metabolism; Trophoblasts - metabolism; Trophoblasts - microbiology
• ISSN: 1933-0219; 1935-3456
• DOI: 10.1038/mi.2012.63

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)-1β. The aim of this study was to understand the innate immune pathways involved in trophoblast production of IL-1β 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-1β secretion is associated with the transcription of IL-1β mRNA, the translation and processing of pro-IL-1β, and the activation of caspase-1. In addition, we demonstrate that Ct-induced IL-1β 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-1β secretion in response to a Ct infection.