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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
09:01

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Viral infection causes rapid sensitization to lipopolysaccharide: central role of IFN-alpha beta

A Nansen1, A Randrup Thomsen

  • 1Institute of Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark.

Journal of Immunology (Baltimore, Md. : 1950)
|January 6, 2001
PubMed

Insights

Viral infections can worsen Gram-negative septic shock by increasing tumor necrosis factor-alpha (TNF-alpha) production. This sensitization is primarily mediated by interferon-alpha/beta (IFN-alphabeta), highlighting a new inflammatory pathway.

Area of Science:

  • Immunology
  • Pathogenesis of Septic Shock
  • Viral-Bacterial Interactions

Background:

  • Lipopolysaccharide (LPS) drives Gram-negative septic shock.
  • Concurrent viral infections can alter septic shock outcomes.
  • Understanding these interactions is crucial for managing sepsis.

Purpose of the Study:

  • To investigate how viral infection influences LPS-induced septic shock.
  • To elucidate the cellular and molecular mechanisms of this sensitization.
  • To identify key mediators involved in virus-induced hypersensitivity to LPS.

Main Methods:

  • Mice were infected with vesicular stomatitis virus (VSV) or treated with polyinosinic:polycytidylic acid (a chemical IFN inducer).
  • Tumor necrosis factor-alpha (TNF-alpha) levels were measured.
  • Studies utilized antibody-depleted and gene-targeted mice, including IFN-alphabeta receptor (IFN-alphabetaR)-deficient mice.
  • Recombinant IFN-alphabeta (rIFN-alphabeta) was used for pretreatment.

Main Results:

  • VSV infection and polyinosinic:polycytidylic acid treatment sensitized mice to LPS early post-infection.
  • This hypersensitivity correlated with increased TNF-alpha production.
  • Depletion of NK cells or elimination of IFN-gamma offered partial protection.
  • IFN-alphabetaR deficiency completely abrogated TNF-alpha hyperproduction, indicating IFN-alphabeta's central role.
  • rIFN-alphabeta pretreatment mimicked the sensitizing effect of viral infection.

Conclusions:

  • IFN-alphabeta plays a key proinflammatory role.
  • Viral infections rapidly sensitize to LPS via IFN-alphabeta-mediated priming for augmented TNF-alpha production.
  • This reveals a novel pathway for viral influence on concurrent bacterial infections.

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