Staff Members - Benha University
Ficolin-2 Levels and FCN2 Genetic Polymorphisms as a Susceptibility Factor in Schistosomiasis
• 2012
Publication Information
Authors
Eman Abou Ouf,1,a Olusola Ojurongbe,1,2,a Akeem A. Akindele,2 Olawumi R. Sina-Agbaje,3 Hoang Van Tong,1Adegboyega O. Adeyeba,2 Peter G. Kremsner,1 Jürgen F. J. Kun,1 and TP Velavan1
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publication.type
International
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Abstract
Background. Human ficolin-2 (L-ficolins) encoded by the FCN2 gene are pattern-recognition proteins
involved in innate immunity and are associated with several infectious diseases.
Methods. A Nigerian cohort of 168 Schistosoma haematobium–infected individuals and 192 healthy controls
were examined for functional single-nucleotide polymorphisms in the promoter region (−986G>A, −602G>A,
−4A>G) and in exon 8 (+6424G>T) using real-time polymerase chain reaction.
Results. The FCN2 −986A and −4G alleles were significantly associated with the occurrence of schistosomiasis
(P = .0004 for −986G>A; P = .0001 for −4A>G). The heterozygous genotypes (P = .0006 for −986G>A; P
= .0002 for −4A>G) were observed to be a risk factor for susceptibility to schistosomiasis, whereas the homozygous
genotypes of major alleles (P = .0002 for −986G>A; P = .0001 for −4A>G) were observed to shield against
schistosomiasis. The haplotype AGGG (P = .0002) was observed to be a risk factor for susceptibility to schistosomiasis
compared with controls, and the haplotype GGAG (P = .04) was observed to confer protection compared
with patients. Ficolin-2 serum level was significantly higher in controls (P < .005) and in controls with GGAG
haplotypes (P < .0001).
Conclusions. Our findings demonstrate that FCN2 promoter variants (−986G>A and −4A>G) influence
ficolin-2 serum levels and susceptibility to schistosomiasis.
involved in innate immunity and are associated with several infectious diseases.
Methods. A Nigerian cohort of 168 Schistosoma haematobium–infected individuals and 192 healthy controls
were examined for functional single-nucleotide polymorphisms in the promoter region (−986G>A, −602G>A,
−4A>G) and in exon 8 (+6424G>T) using real-time polymerase chain reaction.
Results. The FCN2 −986A and −4G alleles were significantly associated with the occurrence of schistosomiasis
(P = .0004 for −986G>A; P = .0001 for −4A>G). The heterozygous genotypes (P = .0006 for −986G>A; P
= .0002 for −4A>G) were observed to be a risk factor for susceptibility to schistosomiasis, whereas the homozygous
genotypes of major alleles (P = .0002 for −986G>A; P = .0001 for −4A>G) were observed to shield against
schistosomiasis. The haplotype AGGG (P = .0002) was observed to be a risk factor for susceptibility to schistosomiasis
compared with controls, and the haplotype GGAG (P = .04) was observed to confer protection compared
with patients. Ficolin-2 serum level was significantly higher in controls (P < .005) and in controls with GGAG
haplotypes (P < .0001).
Conclusions. Our findings demonstrate that FCN2 promoter variants (−986G>A and −4A>G) influence
ficolin-2 serum levels and susceptibility to schistosomiasis.