Progressive Control of Streptococcus agalactiae-Induced Innate Inflammatory Response Is Associated with Time Course Expression of MicroRNA-223 by Neutrophils
Autor: | Georges Casimir, Maud Deny, Marta Romano, Olivier Denis, Mustapha Chamekh |
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Rok vydání: | 2020 |
Předmět: |
Chemokines -- metabolism
Male Pneumonia -- genetics -- immunology -- metabolism 0301 basic medicine Chemokine Chemokine CXCL1 -- genetics -- metabolism Neutrophils Chemokine CXCL1 Chemokine CXCL2 Interleukin-1beta Monocytes Mice Chemokine CXCL2 -- genetics -- metabolism 0302 clinical medicine mir-223 Lung innate immunity Host Response and Inflammation biology Sciences bio-médicales et agricoles Cytokines -- metabolism CXCL2 MicroRNAs -- genetics -- metabolism Infectious Diseases medicine.anatomical_structure Cytokines Chemokines medicine.symptom group B streptococcus Streptococcus agalactiae -- immunology -- pathogenicity Immunology Inflammation Macrophages -- metabolism Microbiology Streptococcus agalactiae Inflammation -- metabolism Proinflammatory cytokine 03 medical and health sciences microRNA medicine Animals Neutrophils -- metabolism Innate immune system Tumor Necrosis Factor-alpha Macrophages Monocyte Pneumonia Monocytes -- metabolism miR-223 Mice Inbred C57BL MicroRNAs 030104 developmental biology Lung -- cytology -- immunology -- pathology inflammation biology.protein Tumor Necrosis Factor-alpha -- metabolism Parasitology 030215 immunology |
Zdroj: | Infection and immunity, 88 (12 Infect Immun |
ISSN: | 1098-5522 0019-9567 |
Popis: | Group B streptococcus (GBS) is a human-pathogenic bacterium inducing a strong inflammatory response that may be detrimental for host tissues if not finely regulated. The inflammatory response can be modulated by different molecular mechanisms, among which growing evidence points toward the crucial role of microRNAs (miRNAs). Regarding innate inflammatory response, studies have reported that miR-223 is essential for the control of granulocyte proliferation and activation. Moreover, a number of investigations on miRNA expression profiling performed in various inflammatory settings have revealed that miR-223 is among the top differentially expressed miRNAs. Yet the dynamic pattern of expression of miR-223 in vivo with respect to the evolution of the inflammatory process, especially in microbial infection, remains elusive. In this study, we analyzed the kinetic expression of miR-223 in an inflammatory model of GBS-induced murine pneumonia and looked for correlates with inflammatory markers, including innate cell infiltrates. We found that miR-223 expression is rapidly induced at very early time points (3 to 6 h postinfection [p.i.]) mainly by lung-infiltrating neutrophils. Interestingly, the level of miR-223 accumulating in the lungs remains higher at later stages of infection (24 h and 48 h p.i.), and this correlates with reduced expression of primary inflammatory cytokines and chemokines and with a shift in infiltrating monocyte and macrophage subtypes toward a regulatory phenotype. Transient inhibition of miR-223 by an antagomir resulted in significant increase of CXCL2 expression and partial enhancement of infiltrating neutrophils in GBS-infected lung tissues. This suggests the potential contribution of miR-223 to the resolution phase of GBS-induced acute inflammation. info:eu-repo/semantics/published |
Databáze: | OpenAIRE |
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