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jOURNAL rEVIEW (mAY 2004)

lt.rsv-cLINeXPaLLERGY.2004.PDF DOWNLOAD 

il9.rsv-lANCET.2004.PDF DOWNLOAD  


1. Interleukin-9 production in the lungs of infants with severe respiratory syncytial
    virus bronchiolitis (Lancet 2004;363:1031-7)
2. Eosionophil activation and cysteinyl leukotriene production in infants with
    respiratory syncytial virus bronchiolitis (Clin Exp Allergy 2004;34:555-8)

  Several studies have suggested that infants in whom respiratory syncytial virus (RSV) bronchiolitis develops will have recurrent wheezing and asthma later in childhood and shown a link between RSV infection and asthma. It has been suggested that acute infantile bronchiolitis associated with RSV may share some pathogenic features. Complicating the picture is the question of whether there is a link between RSV infection in infancy and the development of atopy later in childhood. Although evidence exists showing that the development of atopy is more common in children who have had RSV infection in early childhood, it is unknown whether the RSV infection leads to the development of atopy or if these children are "preprogrammed" to develop more severe manifestations of atopy in response to a viral respiratory infection. Interleukin 9, a type 2 cytokine has been proposed as a key cytokine in susceptibility to asthma. McNamara et al. intended to investigate whether interleukin 9 was produced in the lungs of infants with severe RSV disease and if found, from which cells it originated. Interleukin 9 mRNA expression, which persisted over the course of ventilation, was noted in all infants with bronchiolitis.

  In this article, in term infants with RSV bronchiolitis, investigators confirmed large amounts of interleukin 9 mRNA and interleukin 9 protein and neutrophils seem to be the main source of this type 2 cytokine. It has been suggested that interleukin 9 production by neutrophils may contribute to the pathogenesis of RSV disease. These findings may be relevant to other disease processes, including acute asthma exacerbation, in the lung where neutrophils are the predominant inflammatory cell type. ECP is a specific marker of eosinophil activation although leukotrienes can be released from a variety of cells including mast cells, eosinophils and monocytes. Dimova-Yaneva et al. made an attempt to test the associati on between eosinophil activation and cysteinyl leukotriene production in the upper airway secretions of infants with RSV bronchiolitis. In the majority of their subjects with RSV bronchiolitis ECP and LTC4 were detectable in upper airway secretions and were significantly associated with each other. In this clinical setting much of the detected LTC4 within upper airway secretions is likely to originate from the eosinophil, an observation that may have implications for clinical management and for delineation of the underlying mechanisms associated with this illness.


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