Journal article

Leptospiral LPS escapes mouse TLR4 internalization and TRIF-associated antimicrobial responses through O antigen and associated lipoproteins

D Bonhomme, I Santecchia, F Vernel-Pauillac, M Caroff, P Germon, G Murray, B Adler, IG Boneca, C Werts

Plos Pathogens | PUBLIC LIBRARY SCIENCE | Published : 2020

Open access

Abstract

Leptospirosis is a worldwide re-emerging zoonosis caused by pathogenic Leptospira spp. All vertebrate species can be infected; humans are sensitive hosts whereas other species, such as rodents, may become long-term renal carrier reservoirs. Upon infection, innate immune responses are initiated by recognition of Microbial Associated Molecular Patterns (MAMPs) by Pattern Recognition Receptors (PRRs). Among MAMPs, the lipopolysaccharide (LPS) is recognized by the Toll-Like-Receptor 4 (TLR4) and activates both the MyD88-dependent pathway at the plasma membrane and the TRIF-dependent pathway after TLR4 internalization. We previously showed that leptospiral LPS is not recognized by the humanTLR4, ..

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University of Melbourne Researchers

Grants

Awarded by French Government's Investissement d'Avenir program, Laboratoire d'Excellence "Integrative Biology of Emerging Infectious Diseases"


Awarded by Fin de these de science - Fondation pour la recherche medicale (FRM)


Funding Acknowledgements

This study received funding from the French Government's Investissement d'Avenir program, Laboratoire d'Excellence "Integrative Biology of Emerging Infectious Diseases" (grant no ANR 10 LABX 62 IBEID to IB). DB received funding from the Ecole Doctorale Frontieres de l'Innovation en Recherche et Education (FIRE), Programme Bettencourt. IS was supported by the Institut Carnot Pasteur Microbes & Sante ' given to the Pasteur-Paris University PhD program and the "Fin de these de science" number FDT201805005258 granted by "Fondation pour la recherche me ' dicale (FRM)". The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.