There was also no significant difference in IL-8 or TNFα responses to 0–3 h RP between infected and co-infected subjects (IL-8 Z: −0·717, P = 0·473, Figure 1a; TNFα Z: −1·050, P = 0·294, Figure 1b). In contrast to the production of IL-8 and TNFα, 0–3 h RP induced significantly elevated quantities of IL-10 by WB cultures in co-infected subjects (median: 327·4 ng/mL, range: 1124·3) compared with uninfected controls (median: 137·5 ng/mL, range: 486·3; Z: −2·063, P = 0·039; Figure 1c).

The median concentration of IL-10 production in response to 0–3 h RP was also higher in WB from infected (i.e. only positive for S. mansoni) participants (median: 190·7 ng/mL, range: 642·4, Figure 1c) compared

with uninfected controls but this trend did not reach statistical Rapamycin solubility dmso significance (Z: −1·504, P = 0·133, Figure 1c). There was also no significant difference in 0–3 h RP-specific IL-10 secretion between the infected and co-infected groups (Z: −0·436, P = 0·451, Selleckchem VX809 Figure 1c). The control stimulant zymosan induced levels of IL-10, which did not significantly differ between the three groups (Figure 1c). Further analysis of the 0–3 h RP-specific ratio of IL-10 to TNFα revealed that there was a significant increase in the cytokine ratio in response to 0–3 h RP in co-infected subjects (median: 0·039, range: 0·116; Z: −2·800, P = 0·005, Figure 2) compared with uninfected subjects (median: 0·016, range: 0·139). There was no significant difference between the zymosan-specific IL-10 to TNFα ratio in the different groups. These observations reinforce the theory that 0–3 h RP has ‘regulatory’ activity and promotes IL-10 production compared with pro-inflammatory TNFα in schistosome-infected individuals. As cytokine production is likely to be dependent upon the constituent leucocytes in the WB samples, various leucocyte triclocarban classes were enumerated as a proportion of the total leucocyte count in the three infection groups

(uninfected n = 11, S. mansoni single infected n = 11 and co-infected n = 17; Figure 3). Eosinophils were the only leucocyte subset that was significantly affected by infection status (Kruskal–Wallis test, χ2 = 8·375, P = 0·015) with a higher percentage of eosinophils in WB from S. mansoni-infected (median: 10·6%, range: 34·2, Z: −2·331, P = 0·020) and co-infected participants (median: 12·0%, range: 43·2, Z: −2·658, P = 0·008) than in WB collected from uninfected participants (median: 4·7%, range: 20·6). There was no significant difference between the percentage of circulating eosinophils in blood collected from infected and co-infected participants (Z: −0·470, P = 0·638).