Both infection effects were associated also with the up-regulation of eosinophil mediators with potent helminthotoxic functions (RNASE2 [eosinophil-derived neurotoxin] and RNASE3 [eosinophil cationic protein] [32] perhaps indicating an up-regulation of signals promoting eosinophilia (i.e. in conjunction with the elevated production by PBMCs of spontaneous GM-CSF and IL-5 observed in chronic infections) and helminth-killing ability. This evidence concerns the gene IL5 and infection.