SYSTEMIC MODULATION OF PERIPHERAL EOSINOPHILIA (AIR POUCH MODEL) IN SCHISTOSOMA-MANSONI INFECTION

Schistosoma mansoni infection induces in their hosts a marked and sust ained eosinophilia, which is influenced or modulated by complex mechan isms, that vary according to the phase of infection. To address this p henomenon, we used the air pouch (AP) model in control and infected Sw iss webster mice, analyzing the cellular, tissue response and local ex pression of adhesion molecules [CD18 (beta(2)-chain), CD44, ICAM-1 (CD 54), L-selectin (CD62L), CD49d (alpha(4)-chain), LFA1 (CD11a)]. Infect ed animals were studied at 3 (pre-oviposition phase), 7 (acute phase), and 14 (chronic phase) weeks after infection (5-6 mice/period of infe ction). Normal mice were age-matched. Results showed that after egg st imulation, compared with matched controls, the infected mice, at each point of infection, showed a lower eosinophil response in the acute (7 weeks) and chronic phase (14 weeks) of infection. However when the in fected mice were in pre-oviposition phase (3 weeks) their eosinophil r esponse surpassed the control ones. In the AP wall of infected mice, a significant decrease in the expression of ICAM-1 and CD44 in fibrobla stic-like cells and a reduction in the number of CD18 and CD11a in mig ratory cells were observed. The other adhesion molecules were negative or weakly expressed. The results indicated that in the air pouch mode l, in S. mansoni-infected mice: (I) eosinophil response is strikingly down-regulated, during the acute ovular phase; (2) in the pre-oviposit ion phase, in contrast, it occurs an up-regulatory modulation of eosin ophil response, in which the mechanisms are completely unknown; (3) in the chronic phase of the infection, the down modulation of eosinophil response is less pronounced; 4) Down-regulation of adhesion molecules , specially of ICAM-1 appear to be associated with the lower eosinophi l response.