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KMID : 0578320170400120935
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Molecules and Cells
2017 Volume.40 No. 12 p.935 ~ p.944
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Inhibition of Autolysis by Lipase LipA in Streptococcus pneumoniae Sepsis
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Kim Gyu-Lee
Luong Truc Thanh
Park Sang-Sang
Lee Seung-Yeop
Ha Jung-Ah
Nguyen Cuong Thach
Ahn Ji-Hye
Park Ki-Tae
Paik Man-Jeong
Pyo Suhk-Neung
Briles David E.
Rhee Dong-Kwon
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Abstract
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More than 50% of sepsis cases are associated with pneumonia. Sepsis is caused by infiltration of bacteria into the blood via inflammation, which is triggered by the release of cell wall components following lysis. However, the regulatory mechanism of lysis during infection is not well defined. Mice were infected with Streptococcus pneumoniae D39 wild-type (WT) and lipase mutant (ΔlipA) intranasally (pneumonia model) or intraperitoneally (sepsis model), and survival rate and pneumococcal colonization were determined. LipA and autolysin (LytA) levels were determined by qPCR and western blotting. S. pneumoniae Spd_1447 in the D39 (type 2) strain was identified as a lipase (LipA). In the sepsis model, but not in the pneumonia model, mice infected with the ΔlipA displayed higher mortality rates than did the D39 WT-infected mice. Treatment of pneumococci with serum induced LipA expression at both the mRNA and protein levels. In the presence of serum, the ΔlipA displayed faster lysis rates and higher LytA expression than the WT, both in vitro and in vivo. These results indicate that a pneumococcal lipase (LipA) represses autolysis via inhibition of LytA in a sepsis model.
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KEYWORD
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infection, LipA, LytA, sepsis, S. pneumoniae
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