Role of MyD88 and Toll-like receptors 2 and 4 in the sensing of Parachlamydia acanthamoebae.

Détails

ID Serval
serval:BIB_C3E61D584C70
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Role of MyD88 and Toll-like receptors 2 and 4 in the sensing of Parachlamydia acanthamoebae.
Périodique
Infection and immunity
Auteur⸱e⸱s
Roger T., Casson N., Croxatto A., Entenza J.M., Pusztaszeri M., Akira S., Reymond M.K., Le Roy D., Calandra T., Greub G.
ISSN
1098-5522 (Electronic)
ISSN-L
0019-9567
Statut éditorial
Publié
Date de publication
12/2010
Peer-reviewed
Oui
Volume
78
Numéro
12
Pages
5195-5201
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Parachlamydia acanthamoebae is a Chlamydia-related organism whose pathogenic role in pneumonia is supported by serological and molecular clinical studies and an experimental mouse model of lung infection. Toll-like receptors (TLRs) play a seminal role in sensing microbial products and initiating innate immune responses. The aim of this study was to investigate the roles of MyD88, TLR2, and TLR4 in the interaction of Parachlamydia with macrophages. Here, we showed that Parachlamydia entered bone-marrow derived macrophages (BMDMs) in a TLR-independent manner but did not multiply intracellularly. Interestingly, compared to live bacteria, heat-inactivated Parachlamydia induced the production of substantial amounts of tumor necrosis factor alpha (TNF), interleukin-6 (IL-6), and IL-12p40 by BMDMs and of TNF and IL-6 by peritoneal macrophages as well as RAW 264.7 and J774 macrophage cell lines. Cytokine production by BMDMs, which was partially inhibited upon trypsin treatment of Parachlamydia, was dependent on MyD88, TLR4, and, to a lesser extent, TLR2. Finally, MyD88(-/-), TLR4(-/-), and TLR2(-/-) mice were as resistant as wild-type mice to lung infection following the intratracheal instillation of Parachlamydia. Thus, in contrast to Chlamydia pneumoniae, Parachlamydia acanthamoebae weakly stimulates macrophages, potentially compensating for its low replication capacity in macrophages by escaping the innate immune surveillance.

Mots-clé
Animals, Chlamydia Infections/immunology, Chlamydia Infections/microbiology, Chlamydia Infections/pathology, Chlamydiales/immunology, Chlamydiales/physiology, Female, Host-Pathogen Interactions/immunology, Host-Pathogen Interactions/physiology, Interleukin-6/analysis, Interleukin-6/blood, Interleukin-6/physiology, Lung/chemistry, Lung/immunology, Lung/pathology, Macrophages/immunology, Macrophages/microbiology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Myeloid Differentiation Factor 88/immunology, Myeloid Differentiation Factor 88/physiology, Phagocytosis/physiology, Pneumonia, Bacterial/immunology, Pneumonia, Bacterial/microbiology, Pneumonia, Bacterial/pathology, Signal Transduction/physiology, Toll-Like Receptor 2/immunology, Toll-Like Receptor 2/physiology, Toll-Like Receptor 4/immunology, Toll-Like Receptor 4/physiology, Tumor Necrosis Factor-alpha/analysis, Tumor Necrosis Factor-alpha/blood, Tumor Necrosis Factor-alpha/physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
09/12/2010 9:59
Dernière modification de la notice
20/08/2019 15:39
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