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J Virol, January 1998, p. 837-840, Vol. 72, No. 1
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Respiratory Syncytial Virus Infection of Neonatal Monocytes Stimulates Synthesis of Interferon Regulatory Factor 1 and Interleukin-1 (IL-1)-Converting Enzyme and Secretion of IL-1

Ryoh Takeuchi,¹ Hiroyuki Tsutsumi,^1,* Masaya Osaki,¹ Shigemi Sone,¹ Shosuke Imai,² and Shunzo Chiba¹

Department of Pediatrics, Sapporo Medical University School of Medicine,¹ and Department of Virology, Cancer Institute, Hokkaido University School of Medicine,² Sapporo, Japan

Received 7 July 1997/Accepted 3 October 1997

Interleukin-1 (IL-1) production in response to respiratory syncytial virus (RSV) was investigated in normal neonate monocytes. Intracellular or culture supernatant IL-1 protein levels were measured by enzyme immunoassay. The expression of mRNAs for interferon regulatory factor 1 (IRF-1), IL-1-converting enzyme (ICE), and IL-1 in the cells was analyzed semiquantitatively by reverse transcriptase-PCR. Before RSV exposure, some IRF-1, ICE, and IL-1 transcripts were already expressed in the monocytes. The levels of these transcripts increased significantly 2 h after RSV exposure compared with those in mock-infected cells. At that time, significantly higher intracellular IL-1 protein levels were observed in RSV-exposed cells. After 20 h of RSV exposure, quantities of soluble IL-1 secreted from RSV-exposed cells were moderately higher than those from noninfected cells. These observations suggest that RSV infection of neonatal monocytes triggers enhanced transcription and increased translation of the IL-1 gene and increased secretion of the soluble protein. The later phase of these processes may be promoted by ICE activity, which was upregulated by increased IRF-1. The increase in IRF-1 activity may also result from RSV infection.

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^* Corresponding author. Mailing address: Department of Pediatrics, Sapporo Medical University School of Medicine, Chuoku S-1, W-16, Sapporo 060, Japan. Phone: 81-11-611-2111. Fax: 81-11-611-0352.

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