Autocrine regulation and experimental modulation of interleukin-6 expression by human pulmonary epithelial cells infected with respiratory syncytial virus

Z. Jiang, M. Kunimoto, Janak Patel

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

The mechanisms of regulation of interleukin-6 (IL-6) production in respiratory syncytial virus (RSV)-infected respiratory epithelial cells were evaluated in A549 cell cultures. Incubation with purified RSV resulted in significant production of IL-1α, IL-1β, IL-6, and tumor necrosis factor alpha (TNF-α). Addition of saturating concentrations of neutralizing antibodies against IL-1α, IL-1β, or TNF-α into purified RSV-infected cell cultures resulted in a significant inhibition of IL-6 production, although anti-IL-1α antibody had the most predominant effect (80% inhibition). Anti- IL-1α antibody also almost completely blocked the expression of mRNA for IL- 6. Addition of therapeutic concentrations of dexamethasone (1 μM) or ribavirin (90 μg/ml), an antiviral agent, also significantly inhibited the synthesis of IL-6. Hence, in clinical settings, pharmacological agents such as the specific antagonists of IL-6-inducing cytokines, as well as dexamethasone and ribavirin, could be used to modulate IL-6 production.

Original languageEnglish (US)
Pages (from-to)2496-2499
Number of pages4
JournalJournal of Virology
Volume72
Issue number3
StatePublished - 1998

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Respiratory Syncytial Viruses
interleukin-6
interleukin-1
Interleukin-1
Interleukin-6
epithelial cells
Epithelial Cells
lungs
Lung
viruses
Ribavirin
dexamethasone
Dexamethasone
tumor necrosis factor-alpha
cell culture
Cell Culture Techniques
Tumor Necrosis Factor-alpha
antiviral agents
antibodies
Antibodies

ASJC Scopus subject areas

  • Immunology

Cite this

Autocrine regulation and experimental modulation of interleukin-6 expression by human pulmonary epithelial cells infected with respiratory syncytial virus. / Jiang, Z.; Kunimoto, M.; Patel, Janak.

In: Journal of Virology, Vol. 72, No. 3, 1998, p. 2496-2499.

Research output: Contribution to journalArticle

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