Changes in IgE- and antigen-dependent histamine-release in peripheral blood of Schistosoma mansoni-infected Ugandan fishermen after treatment with praziquantel.
BACKGROUND
Parasite-specific IgE levels correlate with human resistance to reinfection with Schistosoma spp. after chemotherapy. Although the role of eosinophils in schistosomiasis has been the focus of a great deal of important research, the involvement of other Fcepsilon receptor-bearing cells, such as mast cells and basophils, has not been investigated in relation to human immunity to schistosomes. Chemotherapy with praziquantel (PZQ) kills schistosomes living in an in vivo blood environment rich in IgE, eosinophils and basophils. This releases parasite Ags that have the potential to cross-link cell-bound IgE. However, systemic hypersensitivity reactions are not induced by treatment. Here, we describe the effects of schistosomiasis, and its treatment, on human basophil function by following changes in total cellular histamine and in vitro histamine-release induced by schistosome Ags or anti-IgE, in blood samples from infected Ugandan fishermen, who are continuously exposed to S. mansoni infection, before and 1-day and 21-days after PZQ treatment.


RESULTS
There was a significant increase in the total cellular histamine in blood samples at 1-day post-treatment, followed by a very significant further increase by 21-days post-treatment. In vitro histamine-release induced by S. mansoni egg (SEA) or worm (SWA) Ags or anti-IgE antibody, was significantly reduced 1-day post-treatment. The degree of this reduction correlated with pre-treatment infection intensity. Twenty-1-days post-treatment, SEA-induced histamine-release was still significantly lower than at pretreatment. Histamine-release was not correlated to plasma concentrations of total or parasite-specific IgE, nor to specific IgG4 plasma concentrations.


CONCLUSIONS
The biology of human blood basophils is modulated by S. mansoni infection and praziquantel treatment. Infection intensity-dependent suppression of basophil histamine-release, histamine-dependent resistance to infection, and similarities with allergen desensitisation are discussed as possible explanations of these observations.
Satti
Mohamed Z
MZ
Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK. mohdziada@hotmail.com
Cahen
Pierre
P
Skov
Per S
PS
Joseph
Sarah
S
Jones
Frances M
FM
Fitzsimmons
Colin
C
Hoffmann
Karl F
KF
Reimert
Claus
C
Kariuki
H Curtis
HC
Kazibwe
Francis
F
Mwatha
Joseph K
JK
Kimani
Gachuhi
G
Vennervald
Birgitte J
BJ
Ouma
John H
JH
Kabatereine
Narcis B
NB
Dunne
David W
DW
D000818:Animals; D000871:Anthelmintics / Q000627:therapeutic use*; D000888:Antibodies, Anti-Idiotypic / Q000097:blood; D000947:Antigens, Helminth / Q000097:blood*; D015331:Cohort Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005398:Fisheries; D006632:Histamine / Q000097:blood; D006636:Histamine Release / Q000187:drug effects* / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D008297:Male; D011223:Praziquantel / Q000627:therapeutic use*; D012550:Schistosoma mansoni / Q000187:drug effects / Q000276:immunology; D012555:Schistosomiasis mansoni / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D013050:Spectrometry, Fluorescence; D013997:Time Factors; D014454:Uganda
D000871:Anthelmintics; D000888:Antibodies, Anti-Idiotypic; D000947:Antigens, Helminth; C026408:anti-IgE antibodies; D007073:Immunoglobulin E; D011223:Praziquantel; D006632:Histamine