1Zekry Y, 2Maklad S, 1Saneya Fahmy, 2Riad MM and 1Al-Nagar B.
1Pediatric and 2Microbiology Departments, Faculty of Medicine For Girls, Al-Azhar University.
This current study addresses one of the possible humoral
mechanisms that may participate in the regulation of granulomatous
hypersensitivity and morbidity development in Schistosoma mansoni infected
children. In vitro model of
granuloma formation (IVG), utilizing S. mansoni soluble egg antigen (SEA)
conjugated to polyacrylamide beads, was used to investigate the role of
circulating immune complexes (CIC), isolated by polyethylene glycol from
chronic schistosomiasis plasma, in the modulation of granuloma reactions to
(SEA). Peripheral blood mononuclear cells (PBMC) obtained from active
intestinal, hepatointestinal infected children and adolescents and
control-matched subjects were utilized. The mean ± SEM of granuloma index
(GI) of PBMC from intestinal and hepatointestinal patients were 2.20 ± 0.31
and 2.09 ±
0.16 when treated with chronic schistosomiasis plasma and 3.88 ± 0.16
and 3.84 ±
0.12 when treated with normal plasma respectively. Chronic plasma were able to
suppress the IVG reactions in
intestinal (P<0.005) and hepatointestinal (P<0.001) patients. The
percentage suppression ranged from 24.7 to 64.8 for the intestinal group and
from 20.5 to 69.6 for the hepatointestinal group. Highly significant inhibition
of the IVG reactions were also obtained after treatment of PBMC of the two
groups with the isolated CIC (P<0.001). The mean ± SEM of (GI) was 1.67 +
0.04 and 1.73 + 0.80 for intestinal and hepatointestinal group respectively.
Although, there was no significant difference in the suppression effect of CIC
on cells obtained from younger (<16 years) or older (>16 years) infected
children, yet the suppression effect was significant with higher CIC as
compared with normal plasma (P<0.001). No significant correlation was
detected between the suppression effect of CIC and the intensity of infection
(egg / gm stools) (r =0.042, P>0.05). It is concluded that CIC may have a
role in modulation of granulomatous hypersensitivity reaction to (SEA) and
morbidity development in chronic S.
mansoni infected children.