Abstract
Introduction: Variability in severity of Respiratory Syncytial Virus (RSV) infection is reportedly due to differences in inflammatory response. Objective: To characterize the cytokine response in RSV+ infants aged 0 - 36 months and to relate their responses to disease severity. Methods: Nasopharyngeal aspirations (NPAs) were analyzed for RSV and IL-1, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-1RA, IL-4R, IFN-, sTNFR1, sTNFR2, and TNF-α. Clinical data were collected from the medical records. Results: We included 331 infants of whom 214 were RSV+. In comparison to RSV- infants, they had significantly higher levels of TNF-, IL-6, IL-1, and IFN- (p < 0.05). This also applied to anti-inflammatory cytokine IL-10 levels, but these levels were remarkably lower than levels of TNF-, IL-6, and IL-1. sTNFR1/2 were significantly increased in RSV+ infants. Hospitalized patients had significantly higher levels of TNF-, sTNFR2, and IL-10 (p < 0.05) than non-hospitalized patients. The cytokine response could not be related to disease severity. We found no evidence of a skewed Th1/Th2 immune profile. Conclusion: In acute RSV disease, infected infants’ NPAs contain a significant amount of pro-inflammatory cytokines. Whether this response is beneficial or deleterious remains unanswered. Interpersonal variations in cytokine responses might be linked to an inherited tendency to variations in disease severity.
Highlights
Variability in severity of Respiratory Syncytial Virus (RSV) infection is reportedly due to differences in inflammatory response
A number of findings suggest that the variability in the severity of respiratory syncytial virus (RSV) infections may be rooted in individual differences in inflammatory response [1,2] and not to RSV polymorphisms
In vivo human studies of cytokine levels in airway specimens from RSV+ infants indicate a pronounced production of inflammatory and immunoregulating cytokines such as interleukin (IL-)-2, IL-5, IL-6, IL-8, IL-9, IL-10, IL-11, tumor necrosis factor (TNF), Regulated on Activation Normal T-cell Expressed and Secreted (RANTES), and Eosinophil Cationic Protein (ECP) [11,12,13]
Summary
Variability in severity of Respiratory Syncytial Virus (RSV) infection is reportedly due to differences in inflammatory response. A number of findings suggest that the variability in the severity of respiratory syncytial virus (RSV) infections may be rooted in individual differences in inflammatory response [1,2] and not to RSV polymorphisms (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=genome& Cmd=ShowDetailView&TermToSearch=11728). In vivo human studies of cytokine levels in airway specimens from RSV+ infants indicate a pronounced production of inflammatory and immunoregulating cytokines such as interleukin (IL-)-2, IL-5, IL-6, IL-8, IL-9, IL-10, IL-11, tumor necrosis factor (TNF), Regulated on Activation Normal T-cell Expressed and Secreted (RANTES), and Eosinophil Cationic Protein (ECP) [11,12,13]. The clinical significance has been difficult to ascertain since the majority of these studies report unsystematic measurements of cytokine candidates in small groups of patients. Only a few studies have included an appropriate control group
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