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Macrophage C-type lectin is essential for phagosome maturation and acidification during Escherichia coli-induced peritonitis

Authors
 Wook-Bin Lee  ;  Ji-Jing Yan  ;  Ji-Seon Kang  ;  Lark Kyun Kim  ;  Young-Joon Kim 
Citation
 Biochemical and Biophysical Research Communications, Vol.493(4) : 1491-1497, 2017 
Journal Title
 Biochemical and Biophysical Research Communications 
ISSN
 0006-291X 
Issue Date
2017
MeSH
Animals ; Escherichia coli Infections/immunology* ; Escherichia coli Infections/microbiology ; Hydrogen-Ion Concentration ; Immunity, Innate ; Lectins, C-Type/deficiency ; Lectins, C-Type/genetics ; Lectins, C-Type/immunology* ; Macrophages/immunology* ; Macrophages/metabolism ; Macrophages/microbiology ; Membrane Proteins/deficiency ; Membrane Proteins/genetics ; Membrane Proteins/immunology* ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Peritonitis/immunology* ; Peritonitis/microbiology ; Phagocytosis ; Phagosomes/immunology ; Phagosomes/metabolism ; Phagosomes/microbiology ; Reactive Oxygen Species/metabolism ; Sepsis/immunology ; Sepsis/microbiology
Keywords
Bacterial killing ; E. coli-induced peritonitis ; MCL ; Macrophage ; Phagosome acidification ; Phagosome maturation
Abstract
Sepsis is a life-threatening condition caused by an uncontrolled response to bacterial infection. Impaired bactericidal activity in the host is directly associated with severe sepsis; however, the underlying regulatory mechanism(s) is largely unknown. Here, we show that MCL (macrophage C-type lectin) plays a crucial role in killing bacteria during Escherichia coli-induced peritonitis. MCL-deficient mice with E. coli-induced sepsis showed lower survival rates and reduced bacterial clearance when compared with control mice, despite similar levels of proinflammatory cytokine production. Although the ability of macrophages from MCL-deficient mice to kill bacteria was impaired, they showed normal phagocytic activity and production of reactive oxygen species. In addition, MCL-deficient macrophages showed defective phagosome maturation and phagosomal acidification after E. coli infection. Taken together, these results indicate that MCL plays an important role in host defense against E. coli infection by promoting phagosome maturation and acidification, thereby providing new insight into the role of MCL during pathogenesis of sepsis and offering new therapeutic options.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/161224
DOI
10.1016/j.bbrc.2017.10.018
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부)
Yonsei Authors
김락균(Kim, Lark Kyun)
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Full Text
https://www.sciencedirect.com/science/article/pii/S0006291X17319800
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