Rhinovirus Viremia in Children with Respiratory Infections

Xatzipsalti, Maria; Kyrana, Serena; Tsolia, Mariza; Psarras, Stelios; Bossios, Apostolos; Laza-Stanca, Vasile; Johnston, Sebastian L.; Papadopoulos, Nikolaos G.

doi:10.1164/rccm.200502-315oc

Cited by 102 publications

(88 citation statements)

References 25 publications

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“…Epithelial cells in the airways of asthmatics can release even larger amounts of viral RNA than epithelial cells from normal airways, because the impaired synthesis of IFN-␤ in asthmatic epithelial cells allows a greater viral replication and cellular necrosis (not apoptosis) accompanied by membrane disruption (35). It is further supported by the recent finding that the leakage of rhinovirus-derived RNA into the blood during upper respiratory rhinovirus infections is more prominent in asthmatics than nonasthmatics (36). Besides viral RNA, cellular mRNA leaked from, or associated with, necrotic cells is also capable of activating TLR3 with its secondary structures that contain double-stranded sequences (37).…”

Section: Discussionmentioning

confidence: 94%

TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

Niimi

Asano

Shiraishi

et al. 2007

The Journal of Immunology

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Respiratory infections with RNA viruses, such as rhinovirus or respiratory syncytial virus, are a major cause of asthma exacerbation, accompanied by enhanced neutrophilic and/or eosinophilic inflammation of the airways. We studied the effects of dsRNA synthesized during RNA virus replication, and of its receptor, TLR3, on the synthesis of eosinophilic chemokines in bronchial smooth muscle cells (BSMC). Synthetic dsRNA, polyinosinic-cystidic acid (poly(I:C)), induced the synthesis of eosinophilic chemokines, eotaxin-1/CCL11 and RANTES/CCL5, from primary cultures of human BSMC, and IL-4 increased synergistically the synthesis of poly(I:C)-induced CCL11. A robust eosinophil chemotactic activity was released from BSMC stimulated with poly(I:C) and IL-4, which was mostly inhibited by preincubation with an anti-CCL11, but not with an anti-CCL5 Ab. Although the immunoreactivity of TLR3 was detectable on the cellular surface of BSMC by flow cytometric analysis, pretreatment with an anti-TLR3-neutralizing Ab failed to block the poly(I:C)-induced synthesis of CCL11. We have determined by confocal laser-scanning microscopy that the immunoreactivity of TLR3 was aggregated intracellularly in poly(I:C)-stimulated BSMC, colocalizing with fluorescein-labeled poly(I:C). The synthesis of CCL11 was prominently inhibited by the transfection of TLR3-specific small interfering RNA or by bafilomycin A1, an endosomal acidification inhibitor, further supporting the essential role played by intracellular TLR3 in the synthesis of poly(I:C)-induced CCL11 in BSMC. In conclusion, these observations suggest that, by activating intracellular TLR3 in BSMC, respiratory RNA virus infections stimulate the production of CCL11 and enhance eosinophilic inflammation of the airways in the Th2-dominant microenvironment.

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Section: Discussionmentioning

confidence: 94%

TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

Niimi

Asano

Shiraishi

et al. 2007

The Journal of Immunology

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“…Patients with asthma have been shown to have an increased susceptibility to certain viral and bacterial infections (1)(2)(3)(4)(5)(6)(7). Patients with asthma have an increased risk for colonization with certain bacteria, increased risk for latent infections, increased risk for communityacquired pneumonia (7,8), increased morbidity with influenza infection (5), increased likelihood of persistent rhinovirus in the airway epithelium (9,10), and increased risk of invasive infections, such as rhinoviremia and invasive pneumococcal disease (11)(12)(13). This increased risk of colonization, latent infection, infection morbidity, and infection severity may result from underlying immune differences that increase overall susceptibility to infections and asthma in the infant, thus making infants more susceptible to acute infections and to the chronic sequelae of early-life infection.…”

Section: Host Genetic and Familial Determinants Linking Infant Rsv Anmentioning

confidence: 99%

Toward Primary Prevention of Asthma. Reviewing the Evidence for Early-Life Respiratory Viral Infections as Modifiable Risk Factors to Prevent Childhood Asthma

Feldman

Moore

et al. 2015

Am J Respir Crit Care Med

173

172

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A first step in primary disease prevention is identifying common, modifiable risk factors that contribute to a significant proportion of disease development. Infant respiratory viral infection and childhood asthma are the most common acute and chronic diseases of childhood, respectively. Common clinical features and links between these diseases have long been recognized, with early-life respiratory syncytial virus (RSV) and rhinovirus (RV) lower respiratory tract infections (LRTIs) being strongly associated with increased asthma risk. However, there has long been debate over the role of these respiratory viruses in asthma inception. In this article, we systematically review the evidence linking early-life RSV and RV LRTIs with asthma inception and whether they could therefore be targets for primary prevention efforts.

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“…1) [64]. RVs are also able to pass into the bloodstream, causing viraemia, more frequently during acute and severe asthma exacerbations [65].…”

Section: Mechanisms Of Virus-induced Exacerbationmentioning

confidence: 99%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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Respiratory infections have been implicated in the origin and exacerbation of asthma in a variety of ways; however, systemisation of this knowledge in a way helpful for disease management remains suboptimal.Several conceptual issues need to be taken into account: the fact that the effects of an infection may vary according to genetic background, the current immune status of the host, and parallel environmental stimuli, in addition to the particular infectious agent itself. Moreover, childhood is a very special period because of the continuous processes taking place, such as neural, immune and respiratory maturation.Epidemiological studies have convincingly demonstrated that the majority of asthma exacerbations, in both adults and children, follow viral upper respiratory tract infections. Asthma exacerbations are still often unresponsive to current asthma treatment, and new therapeutic approaches are required.This review presents current knowledge on the associations between infection and exacerbation of established asthma with respect to definitions, epidemiology, mechanisms and treatment.

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Rhinovirus Viremia in Children with Respiratory Infections

Abstract: Viremia may occur during RV respiratory infections in normal children and is rather common in the early course of acute asthma exacerbations, suggesting that rhinoviremia may be involved in asthma exacerbation pathogenesis.

Cited by 102 publications

References 25 publications

TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

Toward Primary Prevention of Asthma. Reviewing the Evidence for Early-Life Respiratory Viral Infections as Modifiable Risk Factors to Prevent Childhood Asthma

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

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