A cautionary note on experimental artefacts induced by fetal calf serum in a viral model of pulmonary eosinophilia.

In BALB/c mice, sensitization with the attachment protein (G) of respiratory syncytial virus (RSV) leads to CD4(+) T cell-mediated lung eosinophilia during subsequent challenge with RSV. In this study, we originally intended to test whether activation of RSV-specific cytotoxic T cells by peptide-pulsed dendritic cells (DC) after G protein sensitization could prevent this eosinophilic response. Peptide-pulsed dendritic cells activated CTL, which could mediate protective immunity to RSV. However, DC vaccination aggravated, rather than prevented, pulmonary eosinophilia in G-sensitized mice and also enhanced weight loss upon RSV infection. This was accompanied by preferential pulmonary recruitment of CD4(+) T cells secreting IL-5. The same enhanced Th2-mediated eosinophilic response could be observed in mice that received unloaded dendritic cells and this response occurred even in the absence of prior G sensitization. Since both dendritic cells and RSV were grown in fetal calf serum (FCS)-containing medium, we suspected that FCS had provoked this response. Indeed, neither eosinophilia nor enhanced pathology were observed in mice treated with DC raised in mouse serum. This observation calls for meticulous controls for artefacts induced by fetal calf serum particularly in mouse models of allergic responses of the respiratory tract.