Respiratory Syncytial Virus Induces the Expression of 5-Lipoxygenase and Endothelin-1 in Bronchial Epithelial Cells

doi:10.1006/bbrc.1998.9537

Biochemical and Biophysical Research Communications

Volume 251, Issue 3, 29 October 1998, Pages 704-709

https://doi.org/10.1006/bbrc.1998.9537 Get rights and content

Abstract

Respiratory syncytial virus (RSV) infection causes and exacerbates asthma, yet the mechanism by which RSV triggers asthma is poorly understood. Herein, anin vitromodel of RSV infection was established using HEp-2 and BEAS-2B bronchial epithelial cell lines, and the expression of 5-lipoxygenase (5-LO), and endothelin-1 (ET-1) was examined. RSV infection increased the expression of 5-LO mRNA and protein in both cell lines, as detected by RT-PCR and western blot analysis, respectively. The levels of leukotrienes also increased in the supernatants of RSV infected cells. Furthermore, RSV infection increased the expression of ET-1 mRNA and protein following RSV infection in a time-dependent manner. It is concluded that RSV infection upregulates the expression of ET-1 and 5-LO in the epithelial cells leading to the production of leukotrienes, which may mediate the consequent exacerbation of asthma.

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Citation Excerpt :
Treatment with lipoxin A4 and resolvin E1 (RvDE1) partially restored the alternatively protective macrophage phenotype in the 5-LO-deficient mice (Shirey et al., 2014). RSV infection increase the levels of leukotrienes, 5-LO (Behera et al., 1998), COX-2, and PGE2 (Walker et al., 2021), and treatment with COX-2 inhibitors decreases lung pathology associated with RSV infection (Richardson et al., 2005). Intranasal administration of the SPM, protectin D1 (PD1) and protectin conjugates in tissue regeneration 1 (PCTR1), reduce viral load during RSV infection (Walker et al., 2021).
Resolvin D1 (RvD1), which is biosynthesized from essential long-chain fatty acids, is involved in anti-inflammatory activity and modulation of T cell response. Memory CD8+ T cells are important for controlling tumor growth and viral infections. Exacerbated inflammation has been described as impairing memory CD8+ T cell differentiation. This study aimed to verify the effects of RvD1 on memory CD8+ T cells in vitro and in vivo in a respiratory virus infection model. Peripheral blood mononuclear cells were treated at different time points with RvD1 and stimulated with anti-CD3/anti-CD28 antibodies. Pre-treatment with RvD1 increases the expansion of memory CD8+ T cells. The IL-12 level, a cytokine described to control memory CD8+ T cells, was reduced with RvD1 pre-treatment. When the mTOR axis was inhibited, the IL-12 levels were restored. In a respiratory virus infection model, Balb/c mice were treated with RvD1 before infection or after 7 days after infection. RvD1 treatment after infection increased the frequency of memory CD8+ T cells in the lung expressing II4, II10, and Ifng. During reinfection, RvD1-treated and RSV-infected mice present a high viral load in the lung and lower antibody response in the serum. Our results show that RvD1 modulates the expansion and phenotype of memory CD8+ T cells but contributed to a non-protective response after RSV reinfection.
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¹: Address correspondence to Shyam S. Mohapatra, Ph.D, Division of Allergy and Immunology, Department of Internal Medicine, University of South Florida College of Medicine and VA Hospital, 13000 Bruce B. Downs Blvd., Tampa, FL 33612. Fax: (813) 974-8575. E-mail:[email protected].

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Regular ArticleRespiratory Syncytial Virus Induces the Expression of 5-Lipoxygenase and Endothelin-1 in Bronchial Epithelial Cells

Abstract

J. Pediatr.

J. Pediatr.

J. Allergy Clin. Immunol.

Biochem. Biophys. Res. Commun.

Biochem. Biophys. Res. Commun.

Chest

Biochem. Biophys. Res. Commun.

J. Allergy Clin. Immunol.

Lancet

J. Allergy Clin. Immunol.

J. Allergy Clin. Immonol.

Neuropeptides

Science

Hospital Practice

Pediatr. Pulmonol.

Br. J. Clin. Pharmacol.

Am. Rev. Respir. Dis.

Regular Article
Respiratory Syncytial Virus Induces the Expression of 5-Lipoxygenase and Endothelin-1 in Bronchial Epithelial Cells