Abstract
Respiratory syncytial virus (RSV) is the most important pathogen correlated to the first-time infant wheezing and later recurrence after its primary infection. RSV infection promotes the bronchial smooth muscle sensitivity to leukotrienes (LTs) in acute stage, causes the extensive inflammatory reaction and the aggregation of Th2-like cells during respiratory tract obstruction. Infants and young children infected with RSV exhibit an increased susceptibility to the exposure of exogenous allergens, easy to suffer from the recurrent wheezing, which prompts that the body is still in a state of inflammation or immunological bias. However, the pathological mechanism is unclear. The recent researches demonstrate that abnormal expression of non-coding microRNAs (miRNAs) can be detected from the peripheral blood and airway tract epithelial of RSV infected infants, which participate the regulation of immune cells polarization and LTs synthesis. Improving the immune tolerance can significantly relieve the airway inflammation and broncho-spasm caused by RSV. In this review, we discuss recent advances in understanding the mechanism of RSV-induced inflammatory reaction and immune dysfunction leading to airway hyper-reactivity. Further, we summarize the potential molecular basis that, in this process, miRNAs, which are produced by airway epithelial cells or peripheral blood mononuclear cells, directly or in the form of exosome to regulate the inflammation programs as well as the function, differentiation and proliferation of immune cells. miRNAs may become a potential bio-marker of detecting severe RSV infection and a novel target of early intervention and therapeutic strategy in recurrent wheezing or asthma related to RSV infection.
Highlights
Respiratory syncytial virus (RSV), a single-stranded, negative-sense RNA virus belonging to the genus Orthopneumovirus of the new family Pneumoviridae, is the most common etiological agent for acute lower respiratory infection (ALRI) in infants aged less than 24 months
In infants infected with RSV, the T helper 17 cell (Th17)/regulatory T-cell (Treg) imbalance, and the over-expression of Th2like cytokines make the airway inflammatory reaction getting worse, in preterm newborns, RSV infections are more likely to become severe cases (Mangodt et al, 2015)
airway hyperactivity (AHR) lasts for months or even years after the acute infection stage is one of the significant clinical features in infants primary challenged by RSV, who exhibit an increased susceptibility to the exogenous allergens and reinfection to evoke asthma, especially in those severe enough to cause hospitalization, which is highly associated with the development of asthma and allergic sensitization up to age 7 (Sigurs et al, 2000; Nenna et al, 2015)
Summary
Respiratory syncytial virus (RSV), a single-stranded, negative-sense RNA virus belonging to the genus Orthopneumovirus of the new family Pneumoviridae, is the most common etiological agent for acute lower respiratory infection (ALRI) in infants aged less than 24 months. MiRNA species have recently emerged as gene expression regulators that play a modulatory role in virus infection by modifying host responses in inflammatory and immune cells as well as airway epithelial cells (Globinska et al, 2014; Werz et al, 2017). TSLP, an interleukin-7 (IL-7)-like cytokine derived from epithelial cells, is considered as a master switch in Th2 mediated immune responses, and is believed to play a key role in allergic asthma. It could promote the cytokine production in mast cells and the maturation of dendritic cells (DCs) during the sensitization/priming stage of innate and adaptive allergic responses, while it supports Th2 CD4+T-cell proliferation and induces cytokine production during the challenge stage (Ziegler and Liu, 2006). Initiation of inflammation program, hyper-function of Th2-like cells, as well as decreased immune tolerance, might be the crucial links to wheezing recurrence correlated to RSV infection, while miRNAs participate the regulation of both T-cells function and 5-LO synthesis procedures (Figure 1)
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