Ecto-5′-Nucleotidase (CD73) Deficiency in Mycobacterium tuberculosis-Infected Mice Enhances Neutrophil Recruitment

التفاصيل البيبلوغرافية
العنوان: Ecto-5′-Nucleotidase (CD73) Deficiency in Mycobacterium tuberculosis-Infected Mice Enhances Neutrophil Recruitment
المؤلفون: Grégory Jouvion, Laetitia Petit-Jentreau, Brigitte Gicquel, Patricia Charles, Laleh Majlessi, Ludovic Tailleux
المساهمون: Génétique mycobactérienne - Mycobacterial genetics, Institut Pasteur [Paris] (IP), Université Paris Diderot, Sorbonne Paris Cité, Paris, France, Université Paris Diderot - Paris 7 (UPD7), Histopathologie humaine et Modèles animaux, Pathogénomique mycobactérienne intégrée
المصدر: Infection and Immunity
Infection and Immunity, 2015, 83 (9), pp.3666-3674. ⟨10.1128/IAI.00418-15⟩
بيانات النشر: American Society for Microbiology, 2015.
سنة النشر: 2015
مصطلحات موضوعية: MESH: Mycobacterium tuberculosis, Immunology, MESH: Flow Cytometry, Enzyme-Linked Immunosorbent Assay, Inflammation, MESH: Mice, Knockout, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, Microbiology, Proinflammatory cytokine, 5'-nucleotidase, Mycobacterium tuberculosis, Mice, Immune system, MESH: Mice, Inbred C57BL, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, medicine, Animals, MESH: Animals, MESH: Mice, 5'-Nucleotidase, Tuberculosis, Pulmonary, MESH: Tuberculosis, Pulmonary, Mice, Knockout, Host Response and Inflammation, biology, Purinergic receptor, MESH: Enzyme-Linked Immunosorbent Assay, Flow Cytometry, biology.organism_classification, Adenosine, Mice, Inbred C57BL, MESH: Neutrophil Infiltration, Disease Models, Animal, Infectious Diseases, Neutrophil Infiltration, Female, Parasitology, Tumor necrosis factor alpha, MESH: Disease Models, Animal, medicine.symptom, MESH: 5'-Nucleotidase, MESH: Female, medicine.drug
الوصف: The immune system needs safeguards that prevent collateral tissue damage mediated by the immune system while enabling an effective response against a pathogen. The purinergic pathway is one such mechanism and finely modulates inflammation by sensing nucleotides in the environment. Extracellular ATP is considered to be a danger signal leading to a proinflammatory response, whereas adenosine is immunosuppressive. CD73, also called ecto-5′-nucleotidase, occupies a strategic position in this pathway, as it is the main enzyme responsible for the generation of adenosine from ATP. Here, we explore the role of CD73 during tuberculosis, a disease characterized by an immune response that is harmful to the host and unable to eradicate Mycobacterium tuberculosis . Using CD73 knockout (KO) mice, we found that CD73 regulates the response to M. tuberculosis infection in vitro and in vivo . Mycobacterium-infected murine macrophages derived from CD73 KO mice secrete more keratinocyte chemoattractant (KC), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) and release less vascular endothelial growth factor (VEGF) upon ATP stimulation than do those derived from wild-type (WT) mice. In vivo , CD73 limits the early influx of neutrophils to the lungs without affecting bacterial growth and dissemination. Collectively, our results support the view that CD73 fine-tunes antimycobacterial immune responses.
تدمد: 1098-5522
0019-9567
DOI: 10.1128/iai.00418-15
DOI: 10.1128/IAI.00418-15⟩
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d7f22a9b09377d3786df85828c9bcda9
https://doi.org/10.1128/iai.00418-15
Rights: OPEN
رقم الانضمام: edsair.doi.dedup.....d7f22a9b09377d3786df85828c9bcda9
قاعدة البيانات: OpenAIRE
الوصف
تدمد:10985522
00199567
DOI:10.1128/iai.00418-15