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Updated: Aug 9, 2026

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

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

Published on: December 11, 2013

Respiratory syncytial virus induces prostaglandin E2, IL-10 and IL-11 generation in antigen presenting cells

H Bartz1, F Büning-Pfaue, O Türkel

  • 1Klinik für Kinder und Jugendmedizin der Ruhr Universität im St. Josef Hospital, Bochum, Germany.

Clinical and Experimental Immunology
|August 29, 2002
PubMed

Insights

Respiratory syncytial virus (RSV) infection in infants leads to hospitalization and poor immunity. RSV-infected immune cells release immunosuppressive mediators, potentially explaining the delayed immune response to RSV.

Area of Science:

  • Immunology
  • Virology
  • Pediatrics

Background:

  • Bronchiolitis from respiratory syncytial virus (RSV) frequently hospitalizes infants under one year.
  • RSV infection typically fails to establish protective immunity.
  • Immune cell infiltrates suggest an immune-mediated component in RSV pathogenesis.

Purpose of the Study:

  • To investigate the interaction between RSV and human immune cells (macrophages and dendritic cells).
  • To compare mediator generation in immune cells infected with RSV, parainfluenza virus (PIV3), and influenza virus.
  • To elucidate the role of specific mediators in the host's immune response to RSV.

Main Methods:

  • Human cord blood-derived macrophages and dendritic cells were infected with RSV.
  • Immune cell activation and maturation were assessed via surface antigen expression.
  • Mediator production (cytokines, prostaglandins) was quantified following viral infection or exposure to virus-free supernatant.

Main Results:

  • RSV infection activated macrophages and matured dendritic cells.
  • Live virus infections, unlike cell-free supernatant, induced IL-6 production.
  • RSV infection uniquely stimulated significant IL-10, IL-11, and prostaglandin E2 release from macrophages and dendritic cells.

Conclusions:

  • RSV infection induces specific immune cell responses.
  • RSV-infected macrophages and dendritic cells release immunosuppressive mediators (IL-10, IL-11, PGE2).
  • These mediators may contribute to the lack of protective immunity observed in RSV infections.

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