Recombinant OmpA protein fragments mediate interleukin-17 regulation to prevent Escherichia coli meningitis

Wen Shyang Hsieh, Yi Yuan Yang, Pei Hsuan Lin, Chia Chih Chang, Hsueh Hsia Wu

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: Neonates are at a higher risk for bacterial meningitis than children of other age groups. Although the mortality rates have decreased over the past few decades, neonatal meningitis is still a severe disease with high morbidity. For bacterial meningitis, antibiotic therapy is the primary choice for management. However, neurologic complications often cannot be averted; ~40% of survivors exhibit neurological sequelae. Escherichia coli infection is the common cause of neonatal meningitis. Previously, we have demonstrated that the recombinant loop 1-3, loop 2-3, and loop 2-4 fragments of OmpA protein can protect mice from death after intracerebral E. coli infection. In this study, the protective effects of the recombinant OmpA protein fragments in E. coli intracerebral infections were investigated. Methods: The effects of E. coli intracerebral infection on cytokine and chemokine expression were determined. We also used various recombinant fragments of the OmpA protein to investigate the effects of these recombinant OmpA protein fragments on cytokine and chemokine expression. Results: In this study, we demonstrated that the expression of interleukin-17 and other cytokines, chemokines, inducible nitric oxide synthase, and cyclooxygenase-2 are involved in the inflammatory processes of intracerebral E. coli infection. We also demonstrated that specific recombinant OmpA protein fragments (L1-3, L2-3, L2-4, and L3) can regulate cytokine, chemokine, nitric oxide synthase, and cyclooxygenase-2 expression and, subsequently, protect mice from death caused by intracerebral infection of E. coli. Conclusion: This finding indicates the potential for developing a new therapeutic approach to improve the prognosis of bacterial meningitis.

Original languageEnglish
JournalJournal of Microbiology, Immunology and Infection
Volume49
Issue number6
DOIs
Publication statusPublished - Dec 1 2016

Fingerprint

Escherichia coli Meningitis
Escherichia coli Infections
Interleukin-17
Recombinant Proteins
Chemokines
Bacterial Meningitides
Cytokines
Cyclooxygenase 2
Meningitis
Nitric Oxide Synthase Type II
Nitric Oxide Synthase
Nervous System
Survivors
OMPA outer membrane proteins
Age Groups
Newborn Infant
Anti-Bacterial Agents
Morbidity
Mortality
Therapeutics

Keywords

  • Bacterial meningitis
  • Escherichia coli
  • IL-17
  • NOS-2
  • Outer membrane protein A

ASJC Scopus subject areas

  • Microbiology (medical)
  • Immunology and Allergy
  • Immunology and Microbiology(all)
  • Infectious Diseases

Cite this

Recombinant OmpA protein fragments mediate interleukin-17 regulation to prevent Escherichia coli meningitis. / Hsieh, Wen Shyang; Yang, Yi Yuan; Lin, Pei Hsuan; Chang, Chia Chih; Wu, Hsueh Hsia.

In: Journal of Microbiology, Immunology and Infection, Vol. 49, No. 6, 01.12.2016.

Research output: Contribution to journalArticle

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abstract = "Background: Neonates are at a higher risk for bacterial meningitis than children of other age groups. Although the mortality rates have decreased over the past few decades, neonatal meningitis is still a severe disease with high morbidity. For bacterial meningitis, antibiotic therapy is the primary choice for management. However, neurologic complications often cannot be averted; ~40{\%} of survivors exhibit neurological sequelae. Escherichia coli infection is the common cause of neonatal meningitis. Previously, we have demonstrated that the recombinant loop 1-3, loop 2-3, and loop 2-4 fragments of OmpA protein can protect mice from death after intracerebral E. coli infection. In this study, the protective effects of the recombinant OmpA protein fragments in E. coli intracerebral infections were investigated. Methods: The effects of E. coli intracerebral infection on cytokine and chemokine expression were determined. We also used various recombinant fragments of the OmpA protein to investigate the effects of these recombinant OmpA protein fragments on cytokine and chemokine expression. Results: In this study, we demonstrated that the expression of interleukin-17 and other cytokines, chemokines, inducible nitric oxide synthase, and cyclooxygenase-2 are involved in the inflammatory processes of intracerebral E. coli infection. We also demonstrated that specific recombinant OmpA protein fragments (L1-3, L2-3, L2-4, and L3) can regulate cytokine, chemokine, nitric oxide synthase, and cyclooxygenase-2 expression and, subsequently, protect mice from death caused by intracerebral infection of E. coli. Conclusion: This finding indicates the potential for developing a new therapeutic approach to improve the prognosis of bacterial meningitis.",
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AB - Background: Neonates are at a higher risk for bacterial meningitis than children of other age groups. Although the mortality rates have decreased over the past few decades, neonatal meningitis is still a severe disease with high morbidity. For bacterial meningitis, antibiotic therapy is the primary choice for management. However, neurologic complications often cannot be averted; ~40% of survivors exhibit neurological sequelae. Escherichia coli infection is the common cause of neonatal meningitis. Previously, we have demonstrated that the recombinant loop 1-3, loop 2-3, and loop 2-4 fragments of OmpA protein can protect mice from death after intracerebral E. coli infection. In this study, the protective effects of the recombinant OmpA protein fragments in E. coli intracerebral infections were investigated. Methods: The effects of E. coli intracerebral infection on cytokine and chemokine expression were determined. We also used various recombinant fragments of the OmpA protein to investigate the effects of these recombinant OmpA protein fragments on cytokine and chemokine expression. Results: In this study, we demonstrated that the expression of interleukin-17 and other cytokines, chemokines, inducible nitric oxide synthase, and cyclooxygenase-2 are involved in the inflammatory processes of intracerebral E. coli infection. We also demonstrated that specific recombinant OmpA protein fragments (L1-3, L2-3, L2-4, and L3) can regulate cytokine, chemokine, nitric oxide synthase, and cyclooxygenase-2 expression and, subsequently, protect mice from death caused by intracerebral infection of E. coli. Conclusion: This finding indicates the potential for developing a new therapeutic approach to improve the prognosis of bacterial meningitis.

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