NlpI facilitates deposition of C4bp on Escherichia coli by blocking classical complement-mediated killing, which results in high-level bacteremia

Yu Ting Tseng, Shainn Wei Wang, Kwang Sik Kim, Wang Ying-Hsiang Wang, Yao Yufeng Yao, Chen Chien-Cheng Chen, Chiang Chi-Wu Chiang, Hsieh Pao-Chuan Hsieh, Ching Hao Teng

Research output: Contribution to journalArticle

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Abstract

Neonatal meningitis Escherichia coli (NMEC) is the most common Gram-negative organism that is associated with neonatal meningitis, which usually develops as a result of hematogenous spread of the bacteria. There are two key pathogenesis processes for NMEC to penetrate into the brain, the essential step for the development of E. coli meningitis: a high-level bacteremia and traversal of the blood-brain barrier (BBB). Our previous study has shown that the bacterial outer membrane protein NlpI contributes to NMEC binding to and invasion of brain microvascular endothelial cells, the major component cells of the BBB, suggesting a role for NlpI in NMEC crossing of the BBB. In this study, we showed that NlpI is involved in inducing a high level of bacteremia. In addition, NlpI contributed to the recruitment of the complement regulator C4bp to the surface of NMEC to evade serum killing, which is mediated by the classical complement pathway. NlpI may be involved in the interaction between C4bp and OmpA, which is an outer membrane protein that directly interacts with C4bp on the bacterial surface. The involvement of NlpI in two key pathogenesis processes of NMEC meningitis may make this bacterial factor a potential target for prevention and therapy of E. coli meningitis.

Original languageEnglish
Pages (from-to)3669-3678
Number of pages10
JournalInfection and Immunity
Volume80
Issue number10
DOIs
Publication statusPublished - 2012 Oct 1

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Escherichia coli Meningitis
Bacteremia
Escherichia coli
Blood-Brain Barrier
Meningitis
Bacterial Outer Membrane Proteins
Classical Complement Pathway
Brain
Cellular Structures
Membrane Proteins
Endothelial Cells
Bacteria

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Cite this

Tseng, Yu Ting ; Wang, Shainn Wei ; Kim, Kwang Sik ; Ying-Hsiang Wang, Wang ; Yufeng Yao, Yao ; Chien-Cheng Chen, Chen ; Chi-Wu Chiang, Chiang ; Pao-Chuan Hsieh, Hsieh ; Teng, Ching Hao. / NlpI facilitates deposition of C4bp on Escherichia coli by blocking classical complement-mediated killing, which results in high-level bacteremia. In: Infection and Immunity. 2012 ; Vol. 80, No. 10. pp. 3669-3678.
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abstract = "Neonatal meningitis Escherichia coli (NMEC) is the most common Gram-negative organism that is associated with neonatal meningitis, which usually develops as a result of hematogenous spread of the bacteria. There are two key pathogenesis processes for NMEC to penetrate into the brain, the essential step for the development of E. coli meningitis: a high-level bacteremia and traversal of the blood-brain barrier (BBB). Our previous study has shown that the bacterial outer membrane protein NlpI contributes to NMEC binding to and invasion of brain microvascular endothelial cells, the major component cells of the BBB, suggesting a role for NlpI in NMEC crossing of the BBB. In this study, we showed that NlpI is involved in inducing a high level of bacteremia. In addition, NlpI contributed to the recruitment of the complement regulator C4bp to the surface of NMEC to evade serum killing, which is mediated by the classical complement pathway. NlpI may be involved in the interaction between C4bp and OmpA, which is an outer membrane protein that directly interacts with C4bp on the bacterial surface. The involvement of NlpI in two key pathogenesis processes of NMEC meningitis may make this bacterial factor a potential target for prevention and therapy of E. coli meningitis.",
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NlpI facilitates deposition of C4bp on Escherichia coli by blocking classical complement-mediated killing, which results in high-level bacteremia. / Tseng, Yu Ting; Wang, Shainn Wei; Kim, Kwang Sik; Ying-Hsiang Wang, Wang; Yufeng Yao, Yao; Chien-Cheng Chen, Chen; Chi-Wu Chiang, Chiang; Pao-Chuan Hsieh, Hsieh; Teng, Ching Hao.

In: Infection and Immunity, Vol. 80, No. 10, 01.10.2012, p. 3669-3678.

Research output: Contribution to journalArticle

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T1 - NlpI facilitates deposition of C4bp on Escherichia coli by blocking classical complement-mediated killing, which results in high-level bacteremia

AU - Tseng, Yu Ting

AU - Wang, Shainn Wei

AU - Kim, Kwang Sik

AU - Ying-Hsiang Wang, Wang

AU - Yufeng Yao, Yao

AU - Chien-Cheng Chen, Chen

AU - Chi-Wu Chiang, Chiang

AU - Pao-Chuan Hsieh, Hsieh

AU - Teng, Ching Hao

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