Format

Send to

Choose Destination
J Appl Microbiol. 2016 Nov;121(5):1444-1456. doi: 10.1111/jam.13280.

A phosphoethanolamine transferase specific for the 4'-phosphate residue of Cronobacter sakazakii lipid A.

Liu L1,2, Li Y3,4, Wang X5,6,7, Guo W2.

Author information

1
State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
2
School of Biotechnology, Jiangnan University, Wuxi, China.
3
State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China. yanyanli1123@hotmail.com.
4
Synergetic Innovation Center of Food Safety and Nutrition, Jiangnan University, Wuxi, China. yanyanli1123@hotmail.com.
5
State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China. xwang@jiangnan.edu.cn.
6
School of Biotechnology, Jiangnan University, Wuxi, China. xwang@jiangnan.edu.cn.
7
Synergetic Innovation Center of Food Safety and Nutrition, Jiangnan University, Wuxi, China. xwang@jiangnan.edu.cn.

Abstract

AIMS:

Investigate how Cronobacter sakazakii modify their lipid A structure to avoid recognition by the host immune cells.

METHODS AND RESULTS:

Lipid A modification was observed in C. sakazakii BAA894 grown at pH 5·0 but not pH 7·0. Overexpression of C. sakazakii gene ESA_RS09200 in Escherichia coli W3110 caused a phosphoethanolamine (PEA) modification of lipid A; when ESA_RS09200 was deleted in C. sakazakii BAA894, this lipid A modification disappeared. Lipid A modification was observed in BAA894 grown at pH 5·0 when the 1- phosphate residue of lipid A was removed, but disappeared when the 4'- phosphate residue of lipid A was removed. When ESA_RS16430, the orthologous gene of E. coli pmrA, was deleted in C. sakazakii BAA894, this PEA modification of lipid A was still observed, suggesting that this modification was not regulated by the PmrA-PmrB system. Compared to the wild-type BAA894, ESA_RS09200 deletion mutant showed decreased resistance to cationic antimicrobial peptides (CAMP), increased recognition by TLR4/MD2, decreased ability to invade and persist in mammalian cells.

CONCLUSIONS:

ESA_RS09200 in C. sakazakii BAA894 encodes a PEA transferase that specifically adds a PEA to the 4'-phosphate residue of lipid A, but not regulated by the PmrA-PmrB system. PEA modification of lipid A reduces recognition and killing by the host innate immune system.

SIGNIFICANCE AND IMPACT OF THE STUDY:

This study showed that modification of the lipid A moiety of C. sakazakii with PEA increased resistance to CAMP and recognition of the immune response although signalling of TLR4/MD2 cascade, suggesting that the organism could not successfully evade the host innate immune system without the transference of PEA to its lipid A moiety.

KEYWORDS:

Cronobacter sakazakii ; EptA; lipid A; lipopolysaccharide; phosphoethanolamine transferase

PMID:
27564119
DOI:
10.1111/jam.13280
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center