Your browser doesn't support javascript.
loading
Borrelia burgdorferi Secretes c-di-AMP as an Extracellular Pathogen-Associated Molecular Pattern to Elicit Type I Interferon Responses in Mammalian Hosts.
Priya, Raj; Ye, Meiping; Raghunanadanan, Sajith; Liu, Qiang; Li, Wei; Yu, Qigui; Lou, Yongliang; Sintim, Herman O; Yang, X Frank.
Afiliación
  • Priya R; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
  • Ye M; Department of Dermatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
  • Raghunanadanan S; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
  • Liu Q; National Clinical Laboratory on Tuberculosis, Beijing Key Laboratory for Drug-Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Institute, Beijing, China.
  • Li W; Wenzhou key laboratory of sanitary microbiology, Key Laboratory of Laboratory Medicine, Ministry of Education, School of Laboratory Medicine and Life Sciences, Wenzhou Medical UniversityDepartment of Chemistry, 560 Oval Drive, West Lafayette, IN 47907, USA.
  • Yu Q; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
  • Lou Y; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
  • Sintim HO; Wenzhou key laboratory of sanitary microbiology, Key Laboratory of Laboratory Medicine, Ministry of Education, School of Laboratory Medicine and Life Sciences, Wenzhou Medical UniversityDepartment of Chemistry, 560 Oval Drive, West Lafayette, IN 47907, USA.
  • Yang XF; Institute for Drug Discovery, Purdue University, 720 Clinic Drive, West Lafayette, IN 47907, USA.
bioRxiv ; 2024 Aug 20.
Article en En | MEDLINE | ID: mdl-39185169
ABSTRACT
Borrelia burgdorferi (B. burgdorferi), an extracellular spirochetal pathogen, elicits a type-I interferon (IFN-I) response that contributes to the pathology of Lyme disease, including the development and severity of Lyme arthritis. However, the specific Pathogen-Associated Molecular Patterns (PAMPs) of B. burgdorferi responsible for triggering the IFN-I response are not well understood. Previous studies have identified an unknown, nuclease-resistant component in B. burgdorferi culture supernatants that significantly stimulates the IFN-I response, but its identity remains unknown. In this study, we reveal that B. burgdorferi secretes cyclic-di-adenosine monophosphate (c-di-AMP) as a key extracellular PAMP, inducing the host IFN-I response in macrophages. Using genetically manipulated B. burgdorferi strains, we demonstrate a requirement of c-di-AMP for stimulating IFN-I response by macrophages ex vivo. Additionally, infecting mice with B. burgdorferi alongside exogenous c-di-AMP resulted in a markedly increased IFN-I response in mouse tissues. Furthermore, inactivation or inhibition of the host STING signaling pathway significantly reduced the IFN-I response, indicating that c-di-AMP-induced IFN-I production is STING-dependent. Our findings identify c-di-AMP as a crucial PAMP secreted by B. burgdorferi to elicit the host IFN-I response via activation of STING signaling pathway, suggesting that targeting c-di-AMP production could represent a novel therapeutic strategy against Lyme arthritis.

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: BioRxiv Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: BioRxiv Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos