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Interleukin-1β participates in the development of pneumococcal acute lung injury and death by promoting alveolar microvascular leakage

Title
Interleukin-1β participates in the development of pneumococcal acute lung injury and death by promoting alveolar microvascular leakage
Authors
Bong Y.Shin S.G.Koh S.H.Lim J.H.
Ewha Authors
임재향
SCOPUS Author ID
임재향scopus
Issue Date
2015
Journal Title
Journal of Bacteriology and Virology
ISSN
1598-2467JCR Link
Citation
Journal of Bacteriology and Virology vol. 45, no. 2, pp. 93 - 103
Keywords
Acute lung injuryIL-1R1IL-1βPneumococcusPneumolysinStreptococcus pneumoniae
Publisher
Chonnam National University Medical School
Indexed
SCOPUS; KCI scopus
Document Type
Article
Abstract
Streptococcus pneumoniae (S. pneumoniae, also known as pneumococcus) infections are major causes of death worldwide. Despite the development and use of effective antibiotics, high, early mortality due to pneumococcal infections has not been decreased for the last few decades. Recent study found a deadly hemorrhagic acute lung injury (ALI) as a major cause of death at the early stage of severe pneumococcal infections. Interleukin (IL)-1β was known to play critical roles not only for the development of ALI but also resolution of it. The role of IL-1β on the pathogenesis of pneumococcal ALI, however, has not been well understood yet. This study aims to investigate the role of IL-1β on the development of pneumococcal ALI and subsequent death. IL-1β expression was upregulated in the lungs of pneumococcal ALI in wild-type (WT) mice, but not in the plasma. Despite an increased expression of pulmonary IL-1β, no inflammatory cell infiltration into airway has been observed. Upregulation of IL-1β expression was indeed dependent on pneumococcal cytoplasmic toxin pneumolysin and its cell surface receptor Toll-like receptor 4. Deficiency of IL-1R1, a cell surface receptor of IL-1β, resulted in a markedly reduced hemorrhagic pulmonary edema and early death in pneumococcal ALI. Finally, IL-1β neutralization in WT mice protects against pulmonary hemorrhagic edema and death. These data suggest that pulmonary expression of IL-1β exacerbates pneumolysin-induced ALI and death by promoting alveolar hemorrhagic edema. © 2015, Chonnam National University Medical School. All rights reserved.
DOI
10.4167/jbv.2015.45.2.93
Appears in Collections:
의과대학 > 의학과 > Journal papers
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