Abstract
Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infection in early childhood. Underlying pathomechanisms of elevated pulmonary morbidity in later infancy are largely unknown. We found that RSV‐infected H441 cells showed increased mRNA expression of connective tissue growth factor (CTGF), a key factor in airway remodeling. Additional dexamethasone treatment led to further elevated mRNA levels, indicating additive effects. Caffeine treatment prevented RSV‐mediated increase in CTGF mRNA. RSV may be involved in airway remodeling processes by increasing CTGF mRNA expression. Caffeine might abrogate these negative effects and thereby help to restore lung homeostasis.
Highlights
Respiratory syncytial virus (RSV), a single-strand negative sense RNA virus, is the most important cause of lower respiratory tract infection in early childhood[1]; especially in preterm neonates with chronic lung diseases like bronchopulmonary dysplasia (BPD), these infections can be clinically severe being associated with high morbidity and mortality
As upregulation of Connective tissue growth factor (CTGF) has been detected after mechanical ventilation and hyperoxia in the neonatal lung,[4] in proliferating type II lung epithelial cells, and activated fibroblasts of fibrotic lungs,[5] it has been suggested that CTGF may contribute to BPD
CTGF mRNA levels were further elevated by the addition of dexamethasone in poly(I:C)-transfected cells (36.2 ± 17.1-fold), this was not statistically significant (P = .3992) in comparison with cells transfected with poly(I:C) alone
Summary
Respiratory syncytial virus (RSV), a single-strand negative sense RNA virus, is the most important cause of lower respiratory tract infection in early childhood[1]; especially in preterm neonates with chronic lung diseases like bronchopulmonary dysplasia (BPD), these infections can be clinically severe being associated with high morbidity and mortality. Connective tissue growth factor (CTGF), a downstream mediator of transforming growth factor (TGF)-β, is a matricellular signaling modulator and a key molecule in tissue remodeling.[3] As upregulation of CTGF has been detected after mechanical ventilation and hyperoxia in the neonatal lung,[4] in proliferating type II lung epithelial cells, and activated fibroblasts of fibrotic lungs,[5] it has been suggested that CTGF may contribute to BPD. We recently described increase in CTGF expression by various glucocorticoids in lung epithelial and fibroblast models.[9] In addition, we have shown that TGF-β1-induced upregulation of CTGF can be antagonized by caffeine in A549 lung epithelial cells.[10] As anti-inflammatory agents appear to offer no clinical benefit,[11] the interplay of inflammatory trigger, inflammation, and novel agents positively influencing remodeling processes of the lung is the subject of intense research.
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