Serum IgE determinations and coproparasitological analyses were carried out on 161 individuals from two distinct ethnic groups (Hutus and Twas) from two regions in Rwanda (North and South). The cumulative parasitosis index (calculated for each individual as the sum of the scores for the four most frequent intestinal parasites) shows a linear relation with IgE levels up to a plateau, with no clear pattern of correlation between the score for any given parasite and the IgE level. Such a direct quantitative (but not qualitative) relation reproposes the question on the role of IgE immunoglobulins in intestinal parasitoses.
Several synthetic endothelin (ET) analogues of the C-terminal ET hexapeptide (ET16-21) were analyzed by radio-receptor competition binding assays and biologic activity using both ETA and ETB receptor subtypes. In addition, we produced a hybridoma monoclonal antibody, anti-ET15-21, that appeared to crossreact with the entire ET molecule and was able to neutralize its biologic activity. Antibody binding was measured with competition enzyme-linked immunosorbent assays and a surface plasmon resonance-based biosensor (BIA technology). The ET16-21 moiety was modified with systematic replacement of each residue by alanine (Ala-scan). Whereas the C-terminal residues (Asp18, Ile20, and particularly Trp21) were very important for both receptor binding and immunologic activity, Ala substitution in positions 16, 17, and 19 hardly affected such activities. Analysis of another series of synthetic ET16-21 analogues with the His16 residue replaced by a non-amino-acidic block confirmed that the last two C-terminal residues are essential for receptor and antibody binding, whereas the central region of this hexapeptide is much more tolerant to modification. However, a critical steric conformation of the active hexapeptide is necessary.
Serum IgE levels and IgE antibodies against four intestinal parasites, and the presence and abundance of parasites in stool samples were investigated in 161 Rwanda natives. Most of the IgE turn out to be helminth-reacting antibodies. The stimulation and production of these antibodies are much different from those of anti-amoeba antibodies in their relation to the specific intestinal parasite load; helminth infestations seem to play a major role in the development of anti-amoeba antibodies as well.
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