Increased Nasal Interleukin-33 in the Infants with Acute Respiratory Syncytial Virus Bronchiolitis

양승호,; 추미애,; 박혜진,; 이계향,; 김우택,; 정혜리,

doi:10.7581/pard.2012.22.4.383

Cited by 2 publications

(2 citation statements)

References 25 publications

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“…Cytokines and chemokines produced in experimental primary culture of differentiated pediatric airway epithelial cells largely mirror those present in the airway secretions of infants with severe RSV infection (181,182). Infected epithelial cells can also produce Th2-promoting cytokines IL-33, IL-25, and thymic stromal lymphopoietin (TSLP) (63,145,183,184), and IL-33 has been reported in the airways of infants with acute RSV infection (185).…”

Section: T Cell Responses Chemokines and Cytokines In Infancymentioning

confidence: 95%

Protective and Harmful Immunity to RSV Infection

Openshaw

Chiu

Culley

et al. 2017

Annu. Rev. Immunol.

190

173

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Respiratory syncytial virus (RSV) is an exceptional mucosal pathogen. It specializes in infection of the ciliated respiratory epithelium, causing disease of variable severity with little or no direct systemic effects. It infects virtually all children by the age of three years and then repeatedly infects throughout life; this it does despite relatively slight variations in antigenicity, apparently by inducing selective immunological amnesia. Inappropriate or dysregulated responses to RSV can be pathogenic, causing disease-enhancing inflammation that contributes to short- and long-term effects. In addition, RSV's importance as a largely unrecognized pathogen of debilitated older people is increasingly evident. Vaccines that induce nonpathogenic protective immunity may soon be available, and it is possible that different vaccines will be optimal for infants; older children; young to middle-age adults (including pregnant women); and elderly persons. At the dawn of RSV vaccination, it is timely to review what is known (and unknown) about immune responses to this fascinating virus.

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Section: T Cell Responses Chemokines and Cytokines In Infancymentioning

confidence: 95%

Protective and Harmful Immunity to RSV Infection

Openshaw

Chiu

Culley

et al. 2017

Annu. Rev. Immunol.

190

173

View full text Add to dashboard Cite

show abstract

“…During infection, the airway epithelium is a major source of the "alarmin" cytokine interleukin-33 (IL-33). Intriguingly, nasal aspirates from infants with severe RSV disease have elevated levels of 8), and variants of the IL-33 receptor gene IL1RL1 are associated with severe RSV disease in human infants (9). Immediately following RSV infection in neonatal mice, a robust IL-33 response is elicited in CD45 Ϫ EpCam ϩ pneumocytes (7); this type of response to RSV infection does not occur in adult mice, suggesting age-dependent regulation of IL-33 expression in the lung.…”

mentioning

confidence: 99%

Crawling with Virus: Translational Insights from a Neonatal Mouse Model on the Pathogenesis of Respiratory Syncytial Virus in Infants

You

Saravia

Siefker

et al. 2016

J Virol

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The infant immune response to respiratory syncytial virus (RSV) remains incompletely understood. Here we review the use of a neonatal mouse model of RSV infection to mimic severe infection in human infants. We describe numerous age-specific responses, organized by cell type, observed in RSV-infected neonatal mice and draw comparisons (when possible) to human infants. R espiratory syncytial virus (RSV) is the most common cause of lower respiratory tract infections in infants, and severe RSV disease during infancy is associated with an increased risk of asthma development. The medical and economic burdens of RSV infection are enormous. In the United States alone, there are 85,000 to 144,000 annual hospitalizations with $2.6 billion in associated estimated medical cost (1). Despite its continued impact on global health, RSV remains without a vaccine or adequate therapeutic.While prematurity, immunodeficiency, and congenital heart or chronic lung diseases are risk factors for severe RSV disease, the majority of the infants requiring hospitalization were previously healthy and less than 6 months of age (2), suggesting that age at the time of initial infection is an important predictive factor for disease severity. Therefore, our grasp of severe RSV disease in infants is inevitably tied to our understanding of developmental immunity during the first year of life.The neonatal mouse model of RSV infection has been an invaluable tool for RSV research (3, 4). Briefly, neonatal mice (Յ7 days of age) are infected with RSV and then reinfected 4 weeks later as adults. Compared to mice initially infected as adults, these mice develop the characteristic Th2-biased immunopathologies, including exaggerated pulmonary Th2 cells/cytokines, eosinophilia, mucus hyperproduction, and airway hyperreactivity. In recent years, this model spurred several significant advances in research on how age-dependent differences in various immune and nonimmune cells initiate the immunopathogenesis of RSV infection in infants. This article will briefly discuss said advances, organized by the cell types involved in responding to RSV. EPITHELIAL CELLSThe major cellular target of RSV is airway epithelial cells. In the lower respiratory tract, RSV infects bronchiolar and alveolar (type I and II) epithelial cells (5) and similar cells in mice (6). During infection, the airway epithelium is a major source of the "alarmin" cytokine interleukin-33 (IL-33). Intriguingly, nasal aspirates from infants with severe RSV disease have elevated levels of 8), and variants of the IL-33 receptor gene IL1RL1 are associated with severe RSV disease in human infants (9). Immediately following RSV infection in neonatal mice, a robust IL-33 response is elicited in CD45 Ϫ EpCam ϩ pneumocytes (7); this type of response to RSV infection does not occur in adult mice, suggesting age-dependent regulation of IL-33 expression in the lung. Furthermore, the severity of RSV infection (i.e., Th2-mediated immunopathology) is dependent on the levels of IL-33 early during infection. ILC2SMor...

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Increased Nasal Interleukin-33 in the Infants with Acute Respiratory Syncytial Virus Bronchiolitis

Cited by 2 publications

References 25 publications

Protective and Harmful Immunity to RSV Infection

Protective and Harmful Immunity to RSV Infection

Crawling with Virus: Translational Insights from a Neonatal Mouse Model on the Pathogenesis of Respiratory Syncytial Virus in Infants

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