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
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