دورية أكاديمية
أعرض في EDS

Granulocytes act as a niche for Mycobacterium tuberculosis growth.

التفاصيل البيبلوغرافية
العنوان: Granulocytes act as a niche for Mycobacterium tuberculosis growth.
المؤلفون: Lovewell RR; Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA., Baer CE; Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA., Mishra BB; Department of Immunology and Microbial Disease, Albany Medical College, Albany, NY, 12208, USA., Smith CM; Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA., Sassetti CM; Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, 01655, USA. Christopher.sassetti@umassmed.edu.
المصدر: Mucosal immunology [Mucosal Immunol] 2021 Jan; Vol. 14 (1), pp. 229-241. Date of Electronic Publication: 2020 Jun 01.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 101299742 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1935-3456 (Electronic) Linking ISSN: 19330219 NLM ISO Abbreviation: Mucosal Immunol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2023- : [New York, NY] : Elsevier
Original Publication: New York, NY : Nature Pub. Group, c2008-
مواضيع طبية MeSH: Granulocytes/*immunology , Host-Pathogen Interactions/*immunology , Mycobacterium tuberculosis/*immunology , Tuberculosis/*immunology , Tuberculosis/*microbiology, Animals ; Bacterial Load ; Biomarkers ; Chemotaxis, Leukocyte/immunology ; Cytokines/metabolism ; Disease Susceptibility ; Gene Expression Profiling ; Granulocytes/metabolism ; Immunophenotyping ; Inflammation Mediators/metabolism ; Lymphocyte Depletion ; Mice ; Mice, Knockout ; Severity of Illness Index ; Tuberculosis/diagnosis ; Tuberculosis/metabolism
مستخلص: Granulocyte recruitment to the pulmonary compartment is a hallmark of progressive tuberculosis (TB). This process is well-documented to promote immunopathology, but can also enhance the replication of the pathogen. Both the specific granulocytes responsible for increasing mycobacterial burden and the underlying mechanisms remain obscure. We report that the known immunomodulatory effects of these cells, such as suppression of protective T-cell responses, play a limited role in altering host control of mycobacterial replication in susceptible mice. Instead, we find that the adaptive immune response preferentially restricts the burden of bacteria within monocytes and macrophages compared to granulocytes. Specifically, mycobacteria within inflammatory lesions are preferentially found within long-lived granulocytes that express intermediate levels of the Ly6G marker and low levels of antimicrobial genes. These cells progressively accumulate in the lung and correlate with bacterial load and disease severity, and the ablation of Ly6G-expressing cells lowers mycobacterial burden. These observations suggest a model in which dysregulated granulocytic influx promotes disease by creating a permissive intracellular niche for mycobacterial growth and persistence.
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معلومات مُعتمدة: F32 AI120556 United States AI NIAID NIH HHS; P01 AI132130 United States AI NIAID NIH HHS
المشرفين على المادة: 0 (Biomarkers)
0 (Cytokines)
0 (Inflammation Mediators)
تواريخ الأحداث: Date Created: 20200603 Date Completed: 20211012 Latest Revision: 20240804
رمز التحديث: 20240804
مُعرف محوري في PubMed: PMC7704924
DOI: 10.1038/s41385-020-0300-z
PMID: 32483198
قاعدة البيانات: MEDLINE
الوصف
تدمد:1935-3456
DOI:10.1038/s41385-020-0300-z