Diminished Expression Of Intercellular Adhesion Molecule-1 (ICAM-1) By Monoclonal Antibodies To Interferon Gamma And Interleukin-4 In Schistosoma mansoni Infection.

1Maklad S; 2Moustafa AA; 2Salem AM; 2Riad M; 2Abdel Ghaffar AB; 3Phillips SM and 1El-Sheikh N.

1Microbiology Department, Faculty of Medicine for Girls, Al Azhar University, 2Biochemistry Department, Faculty of Science, Ain Shams University, Cairo, Egypt, 3Allergy and Immunology Division, Faculty of Medicine, University of Pennsylvania, USA.

Cytokines are known to play a pivotal role in schistosomiasis. Adhesion molecules are also important in the disease associated inflammatory responses. The aim of this study was to analyze the influence of Th1/Th2 cytokines on expression of intercellular adhesion molecule-1 (ICAM-1) and granuloma formation in murine S. mansoni infection. Spleen cells obtained from 10 wk infected mice were pretreated with specific monoclonal antibodies (mAb) to Interferon gamma (IFN-gamma) and Interleukin-4 (IL-4). In order to examine the influence of these mAb on the granuloma formation, cells were further cultured with soluble egg antigen (SEA) coated synthetic beads in an in vitro granuloma formation (IVG) assay. Cytospin smears of treated and untreated cells were stained for ICAM-1 and positive immunofluorescence signals were assessed by image analyzer. The percent inhibition in granuloma index (G.I.) was 54.60% and 55.08% for anti IFN-gamma and anti IL-4 treated cells, respectively. The intensity of ICAM-1 expression (unit/cell) was significantly reduced in cells treated with anti-IFN-gamma (4.68) (p<0.005) and anti- IL-4 mAb (4.98) (p<0.005) as compared to that for untreated cells (11.98) and cells treated with isotype negative control (11.23). Significant reduction in the percent number of cells expressing ICAM-1 was demonstrated in anti-IL-4 (p<0.001) but not anti-IFN-g treated cells. The simultaneous inhibition of ICAM-1 and G.I. support the overview that IFN-gamma and IL-4 cytokines have an up-regulatory effect on the ICAM-1 molecules and that expression of these molecules are crucial for cell-cell interactions in immune responses to the parasite.