Contrasting cellular responses in Schistosoma haematobium infected and exposed individuals from areas of high and low transmission in Zimbabwe.
The study compared cytokine profiles of individuals from two areas with different transmission patterns for Schistosoma haematobium. One area was a high transmission (HT) while the other was a low transmission (LT) area for S. haematobium. Observations on cellular immune responses were made on stimulated peripheral blood mononuclear cells (PBMC), which were collected pre-treatment, then at 12 and 18 months post treatment. Stimulation was with schistosome worm and egg antigens and a mitogen, phaetohaemaglutinin (PHA). Observations were made on PBMC proliferation and the profiles of cytokine produced over a 5-day incubation period. The two distinct areas showed significant differences on both levels of proliferation and cytokine production for all the measured classes (IL-4, IL-5, IL-10 and IFN-gamma). PBMC from individuals from the LT area had high levels of proliferation but low cytokine production to both antigen stimulants while PBMC from individuals from the HT area showed low levels of proliferation but high cytokine production levels. Prior to treatment, individuals not excreting schistosome ova in the HT area had higher levels of proliferation to the stimulants, than the infected individuals. However, after treatment re-infected individuals showed high levels of proliferation. Before treatment, both infected and uninfected groups showed low and similar ratios, respectively, of IL-4:IFN-gamma, IL-5:IFN-gamma and IL-10:IFN-gamma, while IFN-gamma was high in the infected individuals. After treatment the non re-infected had higher levels of IL-4, IL-5 and IL-10, with the infected having high levels of IFN-gamma. Th1-like response dominated during infection with the Th2-like responses dominating post treatment and in uninfected individuals. The results indicated that the cytokine balance determines, in part, susceptibility or resistance to S. haematobium infection.
Mduluza
T
T
Biochemistry Department, University of Zimbabwe, Box MP 167, Mount Pleasant, Harare, Zimbabwe. mduluza@medic.uz.ac.zw
Ndhlovu
P D
PD
Midzi
N
N
Scott
J T
JT
Mutapi
F
F
Mary
C
C
Couissinier-Paris
P
P
Turner
C M R
CM
Chandiwana
S K
SK
Woolhouse
M E J
ME
Dessein
A J
AJ
Hagan
P
P
D000293:Adolescent; D000818:Animals; D002648:Child; D005243:Feces / Q000469:parasitology; D006801:Humans; D007371:Interferon-gamma / Q000097:blood / Q000378:metabolism; D016753:Interleukin-10 / Q000097:blood / Q000378:metabolism; D015847:Interleukin-4 / Q000097:blood / Q000378:metabolism; D015848:Interleukin-5 / Q000097:blood / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D011223:Praziquantel / Q000627:therapeutic use; D015995:Prevalence; D012548:Schistosoma haematobium / Q000276:immunology*; D012553:Schistosomiasis haematobia / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology* / Q000635:transmission*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000378:metabolism; D015030:Zimbabwe / Q000453:epidemiology
D015848:Interleukin-5; D016753:Interleukin-10; D015847:Interleukin-4; D011223:Praziquantel; D007371:Interferon-gamma