Infection with respiratory syncytial virus (RSV) is characteristically associated with airway inflammation in early infancy. Elegant historical information is available to suggest that both full term and prematurely born neonates exhibit inflammatory responses with a conspicuous predominance of eosinophils. In addition, erythema toxicum, a common benign exanthem observed in normal neonates is characterized by self resolving cutaneous infiltrates of eosinophils. Recent studies in vitro have shown that RSV can modulate the biological function of basophils and eosinophils, by inducing release from infected respiratory epithelial cells of chemokines with discrete target-cell selectivity. Infection with RSV has been shown to induce the syntheses of IL-6, IL-8, IL-10, GM-CSF, IL-1, MIP 1α, RANTES, IFN-β, TNF-α, TGF-β1 and β2 by the epithelial cells. Synthesis of IL-4, IFN-γ, IL-3, IL-2, IL-5, and IFN-α, appear to be conspicuously absent by epithelial cells after RSV infection. However, these cytokines are often detected in the respiratory secretions secondary to the activation of T cell subsets TH1 or TH2. Based on the available evidence it appears that mucosal infections initiate release of soluble mediator(s) in sequential patterns from cells in mucosal epithelium; cytokine and chemokine release results in recruitment of other cellular elements to mucosal epithelium which in turn, release other proinflammatory or immunoregulatory cytokines; regulation of immune response (development of IgE, IgA, or acquisition of oral tolerance), and expression of cell surface receptors such as MHC Class I or II, ICAM-1, E-Selection, VCAM-1, and other adhesion molecules may be determined by the nature of cytokine cascades generated. The clinical outcome and the magnitude or quality of immune response is influenced by the nature and the temporal sequence of mediators released secondary to epithelial cell-antigen interaction at the mucosal sites. Thus, the outcome of viral-mucosal tissue interaction may express as (1) mucosal and systemic immunity and protection against disease, (2) mucosal and/or systemic disease, or (3) oral tolerance. The soluble mediators released as the result of cell- virus interaction at the mucosal surface may be the most crucial factors in the subsequent outcome of infection and the development of immune response or immunopathology at the mucosal surfaces.
