Differential cytokine responses from primary human Kupffer cells following infection with wild-type or vaccine strain yellow fever virus

Sara E. Woodson, Alexander Freiberg, Michael R. Holbrook

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Wild-type yellow fever virus (YFV) infections result in a hepatotropic disease which is often fatal, while vaccination with the live-attenuated 17-D strain results in productive infection yet is well-tolerated with few adverse events. Kupffer cells (KCs) are resident liver macrophages that have a significant role in pathogen detection, clearance and immune signaling. Although KCs appear to be an important component of YF disease, their role has been under-studied. This study examined cytokine responses in KCs following infection with either wild-type or vaccine strains of YFV. Results indicate that KCs support replication of both wild-type and vaccine strains, yet wild-type YFV induced a prominent and prolonged pro-inflammatory cytokine response (IL-8, TNF-α and RANTES/CCL5) with little control by a major anti-inflammatory cytokine (IL-10). This response was significantly reduced in vaccine strain infections. These data suggest that a differentially regulated infection in KCs may play a critical role in development of disease.

Original languageEnglish (US)
Pages (from-to)188-195
Number of pages8
JournalVirology
Volume412
Issue number1
DOIs
StatePublished - Mar 30 2011

Fingerprint

Yellow fever virus
Kupffer Cells
Vaccines
Cytokines
Infection
Chemokine CCL5
Virus Diseases
Interleukin-8
Interleukin-10
Vaccination
Anti-Inflammatory Agents
Macrophages
Liver

Keywords

  • IL-10
  • IL-8
  • Kupffer cell
  • RANTES/CCL5
  • TNF-α
  • Yellow fever virus

ASJC Scopus subject areas

  • Virology

Cite this

Differential cytokine responses from primary human Kupffer cells following infection with wild-type or vaccine strain yellow fever virus. / Woodson, Sara E.; Freiberg, Alexander; Holbrook, Michael R.

In: Virology, Vol. 412, No. 1, 30.03.2011, p. 188-195.

Research output: Contribution to journalArticle

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