Vinpocetine Suppresses Streptococcus pneumoniae -Induced Inflammation via Inhibition of ERK1 by CYLD.

Szczegóły
Abstrakt

Tytuł:: Vinpocetine Suppresses Streptococcus pneumoniae -Induced Inflammation via Inhibition of ERK1 by CYLD.
Autorzy:: Komatsu K; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303.
Nam DH; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303.
Lee JY; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303.; College of Pharmacy, Chung-Ang University, Dongjak-gu, Seoul 06974, South Korea; and.
Yoneda G; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303.
Yan C; Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642.
Li JD; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303; .
Źródło:: Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2020 Feb 15; Vol. 204 (4), pp. 933-942. Date of Electronic Publication: 2020 Jan 03.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural
Język:: English
Imprint Name(s):: Publication: Bethesda, MD : American Association of Immunologists
Original Publication: Baltimore : Williams & Wilkins, c1950-
MeSH Terms:: Deubiquitinating Enzyme CYLD/*metabolism
Otitis Media/*drug therapy
Pneumococcal Infections/*drug therapy
Vinca Alkaloids/*pharmacology
Animals ; Cell Line ; Deubiquitinating Enzyme CYLD/genetics ; Disease Models, Animal ; Ear, Middle/cytology ; Ear, Middle/drug effects ; Ear, Middle/immunology ; Epithelial Cells ; Gene Knockdown Techniques ; Humans ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/immunology ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 3/metabolism ; Otitis Media/immunology ; Otitis Media/microbiology ; Pneumococcal Infections/immunology ; Pneumococcal Infections/microbiology ; RNA, Small Interfering/metabolism ; Streptococcus pneumoniae/immunology ; Streptococcus pneumoniae/isolation & purification ; Up-Regulation/drug effects ; Vinca Alkaloids/therapeutic use
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Grant Information:: R01 DC013833 United States DC NIDCD NIH HHS; R01 DC015557 United States DC NIDCD NIH HHS; R01 HL088400 United States HL NHLBI NIH HHS; R01 HL134910 United States HL NHLBI NIH HHS
Substance Nomenclature:: 0 (RNA, Small Interfering)
0 (Vinca Alkaloids)
543512OBTC (vinpocetine)
EC 2.7.11.24 (MAPK3 protein, human)
EC 2.7.11.24 (Mapk3 protein, mouse)
EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
EC 3.4.19.12 (CYLD protein, human)
EC 3.4.19.12 (CYLD protein, mouse)
EC 3.4.19.12 (Deubiquitinating Enzyme CYLD)
Entry Date(s):: Date Created: 20200105 Date Completed: 20200921 Latest Revision: 20210901
Update Code:: 20240104
PubMed Central ID:: PMC8406682
DOI:: 10.4049/jimmunol.1901299
PMID:: 31900337
: Czasopismo naukowe

Otitis media (OM) is the most common bacterial infection in children. It remains a major health problem and a substantial socioeconomic burden. Streptococcus pneumoniae ( S. pneumoniae ) is one of the most common bacterial pathogens causing OM. Innate inflammatory response plays a critical role in host defense against bacterial pathogens. However, if excessive, it has a detrimental impact on the middle ear, leading to middle ear inflammation, a hallmark of OM. Currently, there has been limited success in developing effective therapeutic agents to suppress inflammation without serious side effects. In this study, we show that vinpocetine, an antistroke drug, suppressed S. pneumoniae -induced inflammatory response in cultured middle ear epithelial cells as well as in the middle ear of mice. Interestingly, vinpocetine inhibited S. pneumoniae -induced inflammation via upregulating a key negative regulator cylindromatosis (CYLD). Moreover, CYLD suppressed S. pneumoniae -induced inflammation via inhibiting the activation of ERK. Importantly, the postinfection administration of vinpocetine markedly inhibited middle ear inflammation induced by S. pneumoniae in a well-established mouse OM model. These studies provide insights into the molecular mechanisms underlying the tight regulation of inflammation via inhibition of ERK by CYLD and identified vinpocetine as a potential therapeutic agent for suppressing the inflammatory response in the pathogenesis of OM via upregulating negative regulator CYLD expression.
(Copyright © 2020 by The American Association of Immunologists, Inc.)

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