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• W2034709073 abstract "To the Editors: We read with interest the recent article by Patel et al1 on the different cytokine response profiles associated with respiratory syncytial virus (RSV-) and other virus-induced acute otitis media. The authors reported on a significantly higher concentration of interleukin-6 (IL-6) and other cytokines including MCP-1, IL-10, IFN-γ, and IL-8, when compared with other viruses. Out of 129 samples (89%) IL-6 was found to range between 0.34 and 4035.4 pg/mL with a median of 63.91 measured with the Bio-Plex Human Cytokine 17-Plex Panel (BIO-RAD, Hercules, CA, lower detection limit 0.1 pg/mL). These data were observed in 145 children with a median age of 13.5 months. In 65 cases (45%) a virus was identified and RSV was found in 16 cases (24.6%) by either culture, antigen detection test (not specified by the authors), or serology. The authors revealed significantly higher IL-6 values in the RSV as compared with the non-RSV group (P = 0.010). In contrast, Oda and Yamamoto2 (as cited by the authors) observed significantly lower quantities of IL-6 in the sera of hospitalized children with lower respiratory tract infection caused by RSV (40 children with a mean age 15.1 months) compared with adenovirus infection (23 children with a mean age of 19.6 months). We reported on IL-6 values in a small study including 48 significantly younger infants aged 0.5 to 12 months who were consecutively admitted to the Pediatric Department of the Medical University of Graz due to bronchiolitis during the RSV season of November 2000 to April 2001.3 In 31 infants tested RSV positive by antigen test (Directigen RSV Test; BD Biosciences, San Jose, CA) IL-6 values ranged between 0 and 29 pg/mL (Endogen, Inc., Cambridge, MA, lower detection limit 1 pg/mL). This is again in contrast to the significantly higher values reported by Patel et al.1 In vitro infection of bronchial epithelial cells with RSV and adenovirus resulted in significantly higher concentrations of IL-6, IL-8, and RANTES by RSV than by adenovirus (mean IL-6 values being above 1000 pg/mL between 2 and 48 hours after cell infection).4 This difference between the adenovirus and RSV in the induction of these protein mediators in airway epithelial cells might be explaining the differences in the clinical patterns of both viral infections. The exact molecular mechanisms behind these different cytokine responses induced by adenovirus or RSV need to be elucidated. Innate immunity to RSV also has been reported, as demonstrated by increased concentrations of tumor necrosis factor-α, IL-1β, IL-6, and IL-8 in nasal washings of infants during active infection.5 In contrast to adult cells, in neonatal cells inactivated RSV invoked an innate immune system characterized by reduced levels of IFN-γ and IL-12 and no adaptive cytokines.6 Live virus induced fewer innate and no adaptive immune cytokines, and RSV-induced proliferation was absent in neonatal but positive in adult mononuclear cells. Thus, exposure to RSV did not appear to occur before birth and adaptive immune deficiency or greater innate responses might account for early life RSV-induced illnesses. Recently, RSV was shown to alter toll-like receptor 4 membrane and cytosolic location in live-virus infected human tracheal epithelial cell lines.7 Stimulating RSV-infected epithelial cells with toll-like receptor 4 agonist lipopolysaccharide increased synthesis of IL-6, IL-8, and reduced, regulated on activation, normal T cell expressed and secreted (RANTES) production. Different results of studies reporting on systemic IL-6 values might depend on different age-groups (from the neonate to infants and children to adults), on the localization of RSV infection–eg, upper versus lower respiratory tract–and, critically, on the time window of cytokine determination in regard to the course of disease. Results from in vitro studies in different cell lines represented more homologous cytokine profiles with increased IL-6 values that could be responsible for the association of lipopolysaccharide with persistent wheezing,7 and represent the major mediators correlated with the severity of RSV disease.8 Bernhard Resch, MD Wilhelm Müller, MD Pediatric Department Medical University of Graz Research Unit for Neonatal Infectious Diseases and Epidemiology Graz, Austria" @default.
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• W2034709073 date "2009-10-01" @default.
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• W2034709073 title "Systemic Interleukin-6 Response to Respiratory Syncytial Virus Infection" @default.
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• W2034709073 doi "https://doi.org/10.1097/inf.0b013e3181b6558a" @default.
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