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Long pentraxin PTX3 mediates acute inflammatory responses against pneumococcal infection

Title
Long pentraxin PTX3 mediates acute inflammatory responses against pneumococcal infection
Authors
Koh S.H.Shin S.G.Andrade M.J.Go R.-H.Park S.Woo C.-H.Lim J.H.
Ewha Authors
박성희임재향
SCOPUS Author ID
박성희scopus; 임재향scopus
Issue Date
2017
Journal Title
Biochemical and Biophysical Research Communications
ISSN
0006-291XJCR Link
Citation
vol. 493, no. 1, pp. 671 - 676
Keywords
Acute pneumococcal inflammationCommunity acquired pneumoniaMouse modelPentraxin 3Streptococcus pneumoniae
Publisher
Elsevier B.V.
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Streptococcus pneumoniae is an important human pathogen responsible for more than 2 million deaths annually worldwide. The airway epithelium acts as the first-line of defense against pneumococcal infections by regulating acute inflammation against invading pneumococcus. Despite the intact adaptive immunity, failure in early defense due to loss of pattern recognition receptors (PRRs) and/or acute phase proteins (APPs) results in detrimental damage and death. C-reactive protein (CRP), the first found APP, is a member of the pentraxin family of proteins and an important soluble PRR for pneumococcus. CRP and another short pentraxin, serum amyloid P, are critical for acute defense against pneumococcal infection. However, the role of the long pentraxin PTX3 in regulating pneumococcal infections is unknown. In this study, PTX3 expression was upregulated by pneumococcus in epithelial cells and in lungs of mice. In addition, PTX3 potentiated pneumococcal inflammation; overexpression of PTX3 enhanced pneumococcus-induced cytokine expression, whereas knock-down of PTX3 with siPTX3 inhibited the cytokine expression. Furthermore, PTX3 deficiency indeed ameliorated acute inflammation and protected mice against death following pneumococcal infection. Pneumococcal toxin pneumolysin was responsible for PTX3 expression and upregulated PTX3 expression via JNK MAPK signaling. These data implicate PTX3 as a novel therapeutic target for the control of acute inflammation by pneumococcus. © 2017 Elsevier Inc.
DOI
10.1016/j.bbrc.2017.08.133
Appears in Collections:
의과대학 > 의학과 > Journal papers
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